ライフサイエンスコーパス: infarct size

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

2 ntricular (LV) dysfunction and decreased the infarct size.

3 15.29; P=0.039) at 6 months independently of infarct size.

4 nhancement (LGE) imaging overestimates acute infarct size.

5 myocardial ischemia with reperfusion reduce infarct size.

6 tivation of MMP-12 significantly reduced the infarct size.

7 rvival, better cardiac function, and reduced infarct size.

8 eoxyribonuclease, ST-segment resolution, and infarct size.

9 tors of ST-segment resolution and myocardial infarct size.

10 ased rate of adverse events without reducing infarct size.

11 f colchicine treatment could lead to reduced infarct size.

12 ate reperfusion injury and reduce myocardial infarct size.

13 al 3 days after AMI with QLQX did not change infarct size.

14 on per se contributes to injury and ultimate infarct size.

15 be useful means by which to limit myocardial infarct size.

16 ive oxygen species formation, and myocardial infarct size.

17 ting from day 1 after MI, despite comparable infarct size.

18 d activated macrophages, brain swelling, and infarct size.

19 wild-type into Rag1 knock-out mice increased infarct size.

20 er recovery of postischemic LVDP and smaller infarct size.

21 rfusion of myocardial infarction and reduces infarct size.

22 enhanced endogenous fibrinolysis, to reduce infarct size.

23 cardiac magnetic resonance imaging-assessed infarct size.

24 atification by treatment window and baseline infarct size.

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

26 The primary endpoint was final infarct size.

27 sis, left ventricular ejection fraction, and infarct size.

28 PPCI was not associated with a reduction in infarct size.

29 increased cardiac dysfunction, despite equal infarct sizes.

30 This led to a dramatic reduction in infarct size (13% +/- 4%; p < 0.05 vs other groups) and

31 nce interval, 1.91-3.92; P<0.00001), reduced infarct size (-2.25%; 95% confidence interval, -3.55 to

32 -6.91 to -1.18; P=0.006) and a reduction in infarct size (-2.69%; 95% CI, -4.83 to -0.56; P=0.01).

33 hearts, pig plasma taken after RIPC reduced infarct size (25+/-5% of ventricular mass versus 38+/-5%

34 tly improved survival, cardiac function, and infarct size 4 weeks after MI.

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

36 /=24 mm, deferred stenting reduced the final infarct size (6% LV; IQR: 2% to 18% vs. 13% LV; IQR: 7%

37 rdiomyocytes in vitro and reduced myocardial infarct size (-63%) after ischemia/reperfusion injury in

38 Infarct sizes 72 h after 60 min middle cerebral artery o

39 no significant differences were observed for infarct size (8.6%LV; IQR: 4.0 to 14.7 vs. 7.4%LV; IQR:

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

41 or each species, a Pathology Core (to assess infarct size), a Biomarker Core (to measure plasma cardi

42 ith normoglycemia, but the salvage index and infarct size adjusting for area at risk did not differ b

43 Disruption of the GSTP gene also increased infarct size after coronary occlusion in situ.

44 ed to find therapies that can further reduce infarct size after early intervention.

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

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

47 aracteristics associated with a reduction in infarct size after ST-segment-elevation-myocardial infar

48 intracoronary nitrite infusion did not alter infarct size, although a trend to improved myocardial sa

49 of FL into the infarct border zone decreased infarct size and ameliorated post-myocardial infarction

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

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

52 rgery, both with neutral results in terms of infarct size and clinical outcome, but also both with ma

53 percutaneous coronary intervention (PPCI) on infarct size and clinical outcomes is not well establish

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

55 e, CTRP9-KO mice showed increased myocardial infarct size and elevated expression of inflammatory med

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

57 3F8 preserved cardiac function and decreased infarct size and fibrin deposition in a time-dependent m

58 of ischemic preconditioning that may reduce infarct size and improve mortality in the setting of thr

59 at by timely reperfusion is needed to reduce infarct size and improve the prognosis of patients with

60 Co-administration of SEP and L-Cit decreased infarct size and improved coronary flow rate and cardiac

61 ses (8 and 16 mg/kg) of progesterone reduced infarct size and improved functional deficits in our cli

62 s, decreased leukocyte infiltration, reduced infarct size and improved functional outcome.

63 an effect associated with reduced myocardial infarct size and improved heart function.

64 EA pretreatment reduced infarct size and improved neurological outcomes 24h afte

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

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

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

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

69 vation myocardial infarction (STEMI) reduces infarct size and improves survival.

70 Secondary endpoints were enzymatic infarct size and incidence of ventricular arrhythmias.

71 venous metoprolol before reperfusion reduced infarct size and increased left ventricular ejection fra

72 schemic injury significantly decreased brain infarct size and inflammation, and prevented neurologica

73 cal level, SVPs and CSCs similarly inhibited infarct size and interstitial fibrosis, SVPs were superi

74 ion produced the greatest negative effect on infarct size and left ventricular remodeling and functio

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

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

77 ardial infarction flow </=1, nitrite reduced infarct size and major adverse cardiac event and improve

78 Infarct size and microvascular obstruction (MVO) were qu

79 tive) multiple regression model preanalyzing infarct size and MVO were applied via univariate receive

80 Once infarct size and MVO were dichotomized by using univaria

81 Assessment of infarct size and MVO with cardiac MR imaging soon after

82 rombus NET burden correlated positively with infarct size and negatively with ST-segment resolution,

83 Unexpectedly, myocardial infarct size and neutrophil infiltration/activity 2 days

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

85 SAHA reduced infarct size and partially rescued systolic function whe

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

87 nuclease activity correlated negatively with infarct size and positively with ST-segment resolution.

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

89 However, the intuitive link between infarct size and prognosis has not been convincingly dem

90 combination of cells additively reduced the infarct size and promoted vascular proliferation and art

91 rs, collateral vessel status predicted final infarct size and reperfusion.

92 n fraction, prolonged QT interval, and total infarct size and resulted in improve risk reclassificati

93 technical issues related to determination of infarct size and revascularisation procedure.

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

95 T1 maps underestimated infarct size and transmurality relative to LGE images in

96 T1 maps overestimated infarct size and transmurality relative to LGE images in

97 Treatment with m21G6 significantly reduced infarct size and troponin-T release, and led to marked p

98 lar magnetic resonance imaging overestimates infarct size and underestimates recovery of dysfunctiona

99 artery occlusion, we observed that cerebral infarct sizes and fibrin(ogen) deposition in chimeric mi

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

101 Perfused myocardium, infarct size, and (99m)Tc-HYNIC annexin V uptake were qu

102 BMCs improves LV ejection fraction, reduces infarct size, and ameliorates remodeling in patients wit

103 Microvasculature in peri-infarct area, infarct size, and animal functional recovery were assess

104 s independently predicted reperfusion, final infarct size, and clinical outcome.

105 e pivotal outcome parameters of reperfusion, infarct size, and clinical outcome.

106 vention minimizes myocardial damage, reduces infarct size, and decreases morbidity and mortality.

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

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

109 preserved left ventricular function, limited infarct size, and improved H2S levels in cardiac tissue

110 icantly improved myocardial salvage, reduced infarct size, and improved systolic LV function measured

111 , LV end-systolic and end-diastolic volumes, infarct size, and major adverse cardiac and cerebrovascu

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

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

114 ing to increased myocardial salvage, reduced infarct size, and mitigated left ventricular (LV) remode

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

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

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

118 Infarct size as a percentage of LV mass was reduced by M

119 The primary end point was myocardial infarct size as assessed by cardiac enzymes, troponin I,

120 Primary endpoint was myocardial infarct size as assessed by cardiac magnetic resonance i

121 The relative infarct size (as a proportion to left ventricular myocar

122 ic cells, enhanced fibrotic area, and larger infarct size, as well as reduced angiogenesis.

123 ry and was associated with larger myocardial infarct size assessed at 6 months.

124 farction, cardiac arrhythmia, and myocardial infarct size assessed by cardiac magnetic resonance imag

125 The primary efficacy end point was infarct size assessed by cardiac MRI on day 3 to 5.

126 The primary end point was infarct size assessed by measuring creatine kinase relea

127 Secondary outcomes included infarct size assessed by troponin T release and by cardi

128 ine the strength of the relationship between infarct size assessed early after primary percutaneous c

129 against I/R damage as evidenced by decreased infarct size, attenuated apoptosis, and improved functio

130 n of HSPA12B in transgenic mice (Tg) limited infarct size, attenuated cardiac dysfunction and improve

131 Change in infarct size between baseline (3 days after percutaneous

132 nsient focal ischemia, the inhibitor reduced infarct sizes both 24 hours and 14 days poststroke, with

133 ic pre- and postconditioning not only reduce infarct size but also these manifestations of coronary v

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

135 3 loss were not a result of effects on acute infarct size but were associated with unrestrained fibro

136 ars that have attempted to reduce myocardial infarct size by administration of adjunctive therapies a

137 Reduction of myocardial infarct size by remote ischemic preconditioning (RIPC),

138 cpt4), markedly reduced late, but not early, infarct size by suppressing IGF-1 degradation and, conse

139 ed cardiac function and contraction, reduces infarct sizes, cardiac fibrosis and necrosis, haemorrhag

140 rization was associated with increased total infarct size compared with an IRA-only strategy.

141 f LNA-92a significantly (P<0.05) reduced the infarct size compared with control LNA-treated pigs, whi

142 was associated with larger area at risk and infarct size compared with patients with normoglycemia,

143 arction angina (n=79) had a 50% reduction in infarct size compared with those patients without preinf

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

145 CMR-measured infarct size declined progressively after reperfusion in

146 entricular functional outcome independent of infarct size (Delta ejection fraction: P<0.04, Delta end

147 ompared with gadopentetic acid (Gd-DTPA) for infarct size determination, contrast-to-noise ratio (CNR

148 Infarct size determined by CMR was significantly associa

149 ght, left ventricular ejection fraction, and infarct size did not differ between groups.

150 c preconditioning may result in reduction in infarct size during percutaneous coronary intervention (

151 In all groups, infarct size, edema, HT occurrence and severity, and fun

152 PP1 did not change infarct size, electrocardiographic pattern, or cardiac f

153 Infarct size estimated by peak and area under the curve

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

155 Sorafenib had no effect on infarct size, fibrosis, or post-MI neovascularization.

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

157 osis, improved cardiac function, and reduced infarct size following myocardial infarction.

158 Lastly, 1 significantly reduced infarct size following permanent focal ischemia in a mou

159 ess whether circadian rhythms can affect the infarct size, future study design should not only includ

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

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

162 sis showed correlations between BGL and age, infarct size, heart rate (HR), and NIHSS scores (p </= 0

163 Acute metformin treatment worsened the infarct size, HT, and behavior outcome, whereas insulin

164 Systemic hypothermia may reduce infarct size if established before reperfusion.

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

166 bility of ischemic preconditioning to reduce infarct size in 3 species (at 2 sites/species): mice (n=

167 cetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal model, even when delivere

168 Hyperglycemia resulted in increased infarct size in a mouse model of brain hypoxia-ischemia

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

170 nd some evidence suggests that it can reduce infarct size in acute myocardial infarction and acute is

171 The infarct size in aged and Sirt1(+/-) knockout hearts was

172 chemic preconditioning significantly reduced infarct size in all species and (2) we successfully esta

173 ndria-targeting peptide, was shown to reduce infarct size in animals with myocardial infarction and i

174 tions to improve cardiac function and reduce infarct size in both ischemic and nonischemic cardiomyop

175 ted by homoarginine supplementation, whereas infarct size in GAMT(-/-) mice was decreased compared wi

176 protocols ("CAESAR protocols") for measuring infarct size in mice, rabbits, and pigs in a manner that

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

178 alysis showed significant (34%) reduction of infarct size in miR-155 inhibitor-injected animals at 21

179 Ischemic postconditioning reduces infarct size in most, but not all, studies in patients u

180 Remote ischemic conditioning reduces infarct size in patients undergoing interventional reper

181 Median infarct size in patients who had coronary interventions

182 mic preconditioning cannot be used to reduce infarct size in patients with AMI because its occurrence

183 olol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardia

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

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

186 RIPC reduced infarct size in pigs to 16+/-11% versus 43+/-11% in PLA

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

188 utaneous coronary intervention might improve infarct size in ST-elevated myocardial infarction.

189 ation of intravenous (IV) metoprolol reduces infarct size in ST-segment elevation myocardial infarcti

190 en hyperglycemia upon hospital admission and infarct size in STEMI patients is a consequence of a lar

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

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

193 Myocardial salvage was the final infarct size indexed to the initial area at risk.

194 Myocardial infarct size is a major determinant of left ventricular

195 Infarct size is the main determinant of long-term mortal

196 Hypothermia has been reported to reduce infarct size (IS) in patients with ST-segment elevation

197 r quantified left ventricular (LV) function, infarct size (IS), microvascular obstruction (MO), and m

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

199 strain (GLS), proposed as a novel marker of infarct size, is associated with 3- and 6-month LV dilat

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

201 ioning in patients with AMI reported reduced infarct size, it would be premature to give up on cardio

202 Median infarct size (% left ventricular myocardial mass) was 17

203 monstrated more profound hemiparesis, larger infarct sizes, lower Spetzler neurologic scores and incr

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

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

206 in left ventricular (LV) ejection fraction, infarct size, LV end-systolic volume, and LV end-diastol

207 Infarct size may, therefore, be useful as an endpoint in

208 ser extent (percentage of LV mass) of 1-week infarct size (mean +/- standard deviation: 18% +/- 13 vs

209 s, 75 patients (74.3%) showed a reduction in infarct size (mean change, -21.0+/-17.6%).

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

211 Infarct size, measured by CMR or technetium-99m sestamib

212 Median (25th, 75th percentile) time to infarct size measurement was 4 days (3, 10 days) after S

213 Infarct size measurements showed good agreement between

214 Infarct-size measurements and BMC phenotype and function

215 Total infarct size (median, interquartile range) was similar t

216 Despite similar infarct size, MI-ARNi versus MI-vehicle had lower cardia

217 Whether infarct size modifies intra-arterial treatment effect is

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

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

220 Secondary endpoints included infarct size, myocardial salvage index, and angiographic

221 te the association between hyperglycemia and infarct size, myocardial salvage, and area at risk, and

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

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

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

225 ouse neocortical neuron cultures and reduced infarct size, necrotic injury, and cerebral edema format

226 current stroke models in nonhuman primates, infarct size, neurologic function and survival were eval

227 Notably, blockade of TIM-3 markedly reduces infarct size, neuronal cell death, oedema formation and

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

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

230 iation with poor neurological outcome was an infarct size of 4% or greater of brain volume (odds rati

231 Their transfer did not increase the infarct size of Rag1 knock-out mice, indicating antigen-

232 Infarct sizes of the conditional mutants were compared w

233 e oxygen group had an increase in myocardial infarct size on cardiac magnetic resonance (n=139; 20.3

234 The pre-specified primary endpoint was infarct size on pre-discharge CMR.

235 There was no difference in total infarct size or ischemic burden between treatment groups

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

237 e reperfusion resulted in a 49% reduction in infarct size (P<0.005) and a 61% reduction in troponin-T

238 ent group also had significant reductions in infarct size (P<0.01), increased maximal principle strai

239 nd a 19% reduction in cardiac MRI-determined infarct size (P=0.034) with nitrite.

240 troponin T (P=0.85), or cardiac MRI-assessed infarct size (P=0.254) were evident.

241 CA patency and consequently reduced cerebral infarct sizes (P < .005).

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

243 ted in a significant reduction in myocardial infarct size per area at risk compared with sham-RDN (26

244 A strong graded response was present between infarct size (per 5% increase) and subsequent mortality

245 Infarct size (percent of left ventricle [LV]) by CMR did

246 d contractile recovery, coupled with reduced infarct size, plasma troponin I level, and apoptosis.

247 ated the presence of circadian dependence of infarct size plotting the peak creatine kinase against t

248 62 male Wistar-Hannover rats with a range of infarct sizes, plus 14 sham-operated rats, were examined

249 fever were not significantly associated with infarct size, poor outcome, or death.

250 argeted hs-MB destruction limited myocardial infarct size, preserved left ventricular function and ha

251 FDG uptake was significantly larger than the infarct size quantified by late gadolinium enhancement (

252 h) MSCs with c-kit(+) hCSCs produces greater infarct size reduction compared with either cell adminis

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

254 Multiple regression analysis indicated that infarct size reduction was greater in patients who had a

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

256 strain, attenuated remodeling, and decreased infarct size relative to cardiac-derived stem cells- or

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

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

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

260 points to measure mitochondrial absorbance, infarct size, serum markers and apoptotic index.

261 Infarct size, stress and rest perfusion defects were ind

262 Although the circadian dependence of infarct size supported by previous studies poses an intr

263 with enhanced IL-1beta production and larger infarct size; the latter was abolished after treatment w

264 tenuated cardiomyocyte apoptosis and reduced infarct size, thereby recapitulating the beneficial effe

265 it has become possible to reduce myocardial infarct size through early reperfusion.

266 Yet, ticagrelor reduced infarct size to a significantly greater extent than clop

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

268 olism, and arteriole density, while reducing infarct size, ventricular wall stress, and apoptosis wit

269 tion with fingolimod during acute MI reduced infarct size via the reperfusion injury salvage kinase a

270 Infarct size was 17.2% [15.1-20.6] and 16.1% [10.0-22.2]

271 exed MRI-late gadolinium enhancement-defined infarct size was 18.3 (IQR, 7.6-29.9) mL/1.73 m(2) in th

272 Mean infarct size was 5.4+/-7.1%, and mean troponin concentra

273 Infarct size was assessed by CMR in 1,889 patients (71.8

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

275 Infarct size was decreased in CCs, whereas CPC+MSC and C

276 on between real-time resting defect size and infarct size was good (r=0.97; P<0.001), as was the corr

277 Initial infarct size was identical.

278 Consequently, infarct size was increased and left ventricular function

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

280 Infarct size was measured as the peak creatine kinase le

281 crease in CMR-detected non-IRA MI, but total infarct size was not significantly different from an IRA

282 Infarct size was not significantly related to subsequent

283 The increased infarct size was prevented by treatment with nec-1s, str

284 Two days later, infarct size was quantified.

285 The percent infarct size was reduced from 62.87+/-4.13 to 34.67+/-5.

286 Compared with the MI group, total infarct size was reduced in the MI+unload group (49% ver

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

288 ce were subjected to in vivo I/R, myocardial infarct size was significantly greater in Sestrin2 KO co

289 Both compounds reduced significantly the infarct size when administered at the end of sustained i

290 djunctive therapy further reduced myocardial infarct size when coupled with reperfusion.

291 eceived CDCs 20 minutes after IR had reduced infarct size when measured at 48 hours.

292 infarction (STEMI) has been shown to reduce infarct size when used in conjunction with primary percu

293 s no effect on cardiac function, volumes, or infarct size, when only RCTs (n=9) that used MRI-derived

294 al Infarction was more effective in reducing infarct size, whereas BMC injection between 3 and 10 day

295 The former mainly depends on acute infarct size, whereas long-term functional recovery is a

296 croglia leads to a striking, 60% increase in infarct size, which is reversed by microglial repopulati

297 using combined siRNAs significantly reduced infarct size while improving cardiac function after isch

298 y had 80% power to detect a 4% difference in infarct size with 100 patients per group.

299 ogesterone showed a significant reduction in infarct size with 3- and 6-h delays.

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