ライフサイエンスコーパス: ischemic

1 nce interval, 35.3-38.8]), followed by focal ischemic (41.8% [40.0-43.6]), myopic glaucoma (42.1% [40

2 We prospectively enrolled 120 patients with ischemic, 60 patients with dilated cardiomyopathy, and 3

3 Ischemic acute kidney injury (AKI), a complication that

4 dapagliflozin versus placebo including limb ischemic adverse events (HR, 1.07 [95% CI, 0.90-1.26]) a

5 ions, peripheral revascularization, and limb ischemic adverse events were site-reported and categoriz

6 4-deficient (KO) mice were protected against ischemic AKI with significantly attenuated renal tubular

7 4 antagonist (5-BDBD) were protected against ischemic AKI.

8 e created based on FFR thresholds (<=0.80 as ischemic and >0.80 as nonischemic).

9 y intervention are at increased risk of both ischemic and bleeding complications.

10 ous analytical approaches in assessing total ischemic and bleeding events after percutaneous coronary

11 ticagrelor monotherapy consistently reduced ischemic and bleeding events by 5% to 8%, compared with

12 nsidering the net clinical benefit including ischemic and bleeding events.

13 wn regarding the mechanism and predictors of ischemic and hemorrhagic stroke.

14 fingolimod show promise for the treatment of ischemic and hemorrhagic stroke.

15 cent years, mortality rates remain high when ischemic and hemorrhagic strokes are present.

16 Temporal trends in acute stroke (ischemic and hemorrhagic)/transient ischemic attack inci

17 molecular differences between patients with ischemic and nonischemic HF.

18 Using rat retina RNA-seq data from ischemic and normal conditions, we show that over 74% of

19 only affect the structural properties of the ischemic and post-infarct heart, but they also play a cr

20 rcise efficiently counteracts the metabolic, ischemic, and regenerative deficits of fatty liver.

21 inst cerebral I/R injury by suppressing post-ischemic apoptosis, whereas heavy ethanol consumption ma

22 of vascular damage, and revascularization of ischemic areas in pathologic conditions.

23 cells (HSPCs) stimulate revascularization of ischemic areas.

24 Even eyes that were severely ischemic at baseline had no significant changes in RNP a

25 haemic events were prior stroke or transient ischemic attack (TIA) (HR 1.42, 95% CI 0.96 to 2.10) and

26 ) reduced stroke risk in high-risk transient ischemic attack (TIA) patients assessed by ABCD2 score.

27 r a cryptogenic ischemic stroke or transient ischemic attack (TIA).

28 rticipants with ischemic stroke or transient ischemic attack (TIA).

29 participants with recent stroke or transient ischemic attack and no known coronary heart disease.

30 cause of clinical symptoms such as transient ischemic attack and stroke.

31 stroke (ischemic and hemorrhagic)/transient ischemic attack incidence and in-hospital mortality were

32 scores 4 to 6, previous stroke or transient ischemic attack, age >=75, and no previous coronary arte

33 al coronary heart disease, stroke, transient ischemic attack, heart failure hospitalization, cardiac

34 betes mellitus, previous stroke or transient ischemic attack, vascular disease, 65 to 74 years of age

35 have had recent ischemic stroke or transient ischemic attack.

36 evaluated after ischemic stroke or transient ischemic attack.

37 and outcomes were recurrent stroke/transient ischemic attack/systemic embolism, symptomatic intracere

38 to 20-minute occlusions mimicking transient ischemic attacks (14/19 vs 6/18 with vehicle, relative r

39 between experimental stroke and patients by ischemic blood probing during the hyperacute stage of va

40 atory Ly-6C(Lo) monocytes/macrophages in the ischemic brain along with the reduced neutrophil counts.

41 ut the functions of neuron-derived E2 in the ischemic brain are unclear.

42 idence that immune cells contribute to acute ischemic brain damage and indicate that ischemic inflamm

43 d autophagy are two key elements involved in ischemic brain damage.

44 , and the glutamate transporter, GLT-1 after ischemic brain damage.

45 e most common acute brain injury was hypoxic-ischemic brain injury (44%), followed by intracranial he

46 Patients with hypoxic-ischemic brain injury had more hypertension (8 vs 4; p =

47 mplication, 23% (95% CI, 0.14-0.32%) hypoxic-ischemic brain injury, 6% (95% CI, 0.02-0.11%) ischemic

48 s to relay a neuroprotective signal into the ischemic brain.

49 In patients with an ischemic burden >10%, the CAC-absent group was associate

50 The prognostic value of CAC, beyond ischemic burden, suggests its potential as a first-step

51 d with patients aged less than 70 years with ischemic cardiomyopathy as indicated using logistic regr

52 on) is difficult to predict in patients with ischemic cardiomyopathy either by clinical tools or by a

53 developed and applied retrospectively to 29 ischemic cardiomyopathy patients with contrast-enhanced

54 One hundred twenty-two consecutive ischemic cardiomyopathy patients with left ventricular e

55 ntricular ejection fraction was 20%, 81% had ischemic cardiomyopathy, and PAINESD score was 18+/-5.

56 iovascular disease outcomes in patients with ischemic cardiomyopathy.

57 nance images to predict VAs in patients with ischemic cardiomyopathy.

58 T ablation procedure data from patients with ischemic cardiomyopathy.

59 d novel phenotypes for long-term outcomes in ischemic cardiomyopathy.

60 Ischemic cardiovascular diseases, particularly acute myo

61 l conservative strategy, reduced the risk of ischemic cardiovascular events or death from any cause o

62 both vasodilators can accurately identify an ischemic cause in patients with nonobstructive coronary

63 ique, no history of atrial fibrillation, and ischemic cause.

64 ar carcinomas (HCCs) are treated by inducing ischemic cell death with transarterial embolization (TAE

65 otion of a rapid elevation of O(2) levels in ischemic cells produces high amounts of reactive oxygen

66 ions was observed in the DCD SLK group, with ischemic cholangiopathy being the most common (10.0% vs

67 n compromise colonic blood supply leading to ischemic complications; however, few data exist regardin

68 Remote ischemic conditioning (RIC), transient restriction and r

69 nitors (cFAPs) and show that they respond to ischemic damage by generating fibrogenic cells.

70 sent a therapeutic strategy for treatment of ischemic disorders.

71 icagrelor is associated with maintained anti-ischemic efficacy while protecting these patients agains

72 to the NICU with moderate-to-severe hypoxic-ischemic encephalopathy at day 1 to 5 during hospitaliza

73 unit (NICU) with moderate-to-severe hypoxic-ischemic encephalopathy at day 1 to 5 during hospitaliza

74 guidelines (adult cardiac arrest and hypoxic-ischemic encephalopathy of newborns).

75 , no significant differences in the risks of ischemic end points or major bleeding were observed with

76 tients with chronic coronary artery disease, ischemic episodes lead to a global pattern of cardiomyoc

77 ABA(A) alpha5 antagonist S44819 after Recent ischemic Event (RESTORE BRAIN) aimed to evaluate the saf

78 re were 560 patients who had at least 1 limb ischemic event, 454 patients with at least 1 peripheral

79 mechanical thrombectomy up to 24 h after the ischemic event, there is resurgent interest in neuroprot

80 0.97% [95% CI, 0.23-1.70]) and fewer severe ischemic events (absolute risk difference, -0.91% [95% C

81 nor did they have a lower rate of recurrent ischemic events (vs >14 days; OR = 0.76, 95% CI = 0.36-1

82 While ischemic events clearly result in significant metabolic

83 explore the association between morphine and ischemic events in 5,438 patients treated with concomita

84 Dual antiplatelet therapy reduces ischemic events in cardiovascular disease, but it increa

85 -1beta antibody, prevented the recurrence of ischemic events in patients with prior acute myocardial

86 ery disease (PAD) are at heightened risk for ischemic events related to atherothrombosis.

87 CI, 0.23-2.27]), whereas the risk of severe ischemic events was similar (absolute risk difference, -

88 the tradeoff of risk (bleeding) and benefit (ischemic events) over time with apixaban versus VKA and

89 s might thus aggravate coincidental cerebral ischemic events.

90 holipid peroxidation, has been implicated in ischemic events.

91 largely by reducing de novo atherothrombotic ischemic events.

92 e subtilisin-kexin type 9 inhibitors reduces ischemic events; however, the cost-effectiveness in stat

93 was not altered in the ethanol groups, post-ischemic expression of Bcl-2 was significantly greater i

94 Moreover, although post-ischemic expression of Beclin-1 was not altered in the e

95 In the ischemic FFR cohort, PCI was associated with a significa

96 Among 2693 patients with an ischemic FFR, 75.3% received PCI and 24.7% were treated

97 of encephalomalacia, corresponding to known ischemic foci.

98 e expression dynamics in the mouse blood and ischemic heart at the single-cell level, and reveal a pr

99 l tissue specification of neutrophils in the ischemic heart characterized by the acquisition of a Sig

100 ubstantial health care spending in 2016 were ischemic heart disease ($89.3 billion [95% CI, $81.1-$95

101 Cardiovascular diseases (CVDs), principally ischemic heart disease (IHD) and stroke, are the leading

102 However, their long-term risks of ischemic heart disease (IHD) and whether such risks are

103 g 7,326 major coronary events (MCEs), 37,992 ischemic heart disease (IHD), and 42,951 strokes were re

104 isease, previous myocardial infarction (MI), ischemic heart disease (IHD), heart failure (HF), atrial

105 l hypercholesterolemia (FH) in subjects with ischemic heart disease (IHD), premature IHD, and severe

106 acids (TFAs) are a well-known risk factor of ischemic heart disease (IHD).

107 y-related mortality, and higher incidence of ischemic heart disease among PLWHIV in cohort studies) o

108 e clinical events among patients with stable ischemic heart disease and moderate or severe ischemia.

109 However, mortality due to ischemic heart disease and other somatic diseases decrea

110 ts referred for cardiac CT for evaluation of ischemic heart disease between September 2014 and March

111 Ischemic heart disease is a leading cause of heart failu

112 vascularization improves prognosis in stable ischemic heart disease is controversial.

113 age, 67+/-11.6 years; 88 men) with suspected ischemic heart disease or known coronary disease who had

114 Patients with stable ischemic heart disease remain at substantial risk for lo

115 Ischemic heart disease remains the foremost cause of dea

116 rs, and comorbid conditions of HF (including ischemic heart disease, aortic valve disease, atrial fib

117 e for HIV and the presence of a cough, COPD, ischemic heart disease, pregnancy-related mortality, mat

118 In patients with stable ischemic heart disease, routine revascularization was no

119 ociation was modified by age, sex, and prior ischemic heart disease.

120 onservative strategy in patients with stable ischemic heart disease.

121 clinical workup and therapeutic guidance in ischemic heart disease.

122 in noninflammatory cardiac disease (3.75%), ischemic heart failure (2%), or healthy blood donors (0.

123 etabolic differences between the hypoxic and ischemic hearts.

124 CYC is decreased in the ischemic hemispheres and pCECs from WT but not in miR-34

125 ce had reduced perfusion and angiogenesis in ischemic hind limbs.

126 Panretinal ischemic index did not demonstrate any significant chang

127 Panretinal ischemic index did not improve and trended toward worsen

128 inal leakage index, microaneurysm count, and ischemic index were not significantly different between

129 llowed by intracranial hemorrhage (24%), and ischemic infarct (16%).

130 mptom onset (58.9%), including 17 with acute ischemic infarct (23.3%), one with a deep venous thrombo

131 a variety of brain imaging findings such as ischemic infarct, hemorrhage, and acute hemorrhagic necr

132 rophages and neuronal lineages sensitizes to ischemic infarction by promoting apoptosis.

133 6%); only 16% of these studies showed recent ischemic infarcts or acute bleeding.

134 cute ischemic brain damage and indicate that ischemic inflammation initiates already during vascular

135 The mechanisms of ischemic injury and inflammatory response differ greatly

136 rom bone marrow niches in response to remote ischemic injury and migrate to the areas of damage and s

137 embryonic development and in the context of ischemic injury and neuroinflammation.

138 identify that transvalvular unloading limits ischemic injury before reperfusion, improves myocardial

139 We and others have shown that ischemic injury can induce both nociception-related beha

140 eeded resource, tissue damage from prolonged ischemic injury can result in early allograft dysfunctio

141 therapies to offset cardiomyocyte loss after ischemic injury improve long-term cardiac function despi

142 rdiac remodeling and infarct expansion after ischemic injury in association with greater mitochondria

143 ese two factors conferred protection against ischemic injury in mature mouse hearts that were otherwi

144 d permeability transition pore opening after ischemic injury to reduce ongoing pathological remodelin

145 After ischemic injury to the myocardium, dendritic cells (DC)

146 rdiac injury, and long-term adaptation after ischemic injury.

147 fibrin microthrombi, without universal acute ischemic injury.

148 iators which are generated during myocardial ischemic injury.

149 a in neurons and are protected from cerebral ischemic injury.

150 ar (caSMC and caEC) mechanisms in myocardial ischemic injury.

151 brain enters the tissue within minutes of an ischemic insult along perivascular flow channels.

152 educing complement-mediated damage following ischemic insult.

153 e dose, complement activation and acute post-ischemic kidney injury are prevented, with additional pr

154 tly associated with a lower rate of MACE for ischemic lesions and a higher rate of MACE for nonischem

155 projections to both hemispheres of rats with ischemic lesions in the cerebral cortex.

156 SBP was associated with an increased risk of ischemic limb events.

157 tion reduced histological injury of the post-ischemic lung and reduced mortality from 55 to 9%.

158 ombination significantly hastened healing in ischemic methicillin-resistant Staphylococcus aureus inf

159 nced claudin-5 mRNA and protein abundance in ischemic mouse brains.

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

161 nsequently, fewer leukocytes migrated to the ischemic myocardium.

162 our glaucoma phenotypes were assessed: focal ischemic (n = 45), generalized cup enlargement (n = 60),

163 Characterizing acute ischemic neuronal activity dynamics is important for und

164 orted in patients with nonarteritic anterior ischemic optic neuropathy (NA-AION).

165 led, 27 with NTG and 54 with NGON, including ischemic optic neuropathy, previous optic neuritis, and

166 Patients with ischemic or dilated cardiomyopathy and reduced left vent

167 ysis of HF decellularized ECM resulting from ischemic or dilated cardiomyopathy, as well as from mous

168 M result in altered mechanical properties of ischemic or infarcted myocardial segments.

169 striction (DR) may prevent organ damage from ischemic or toxic insults in animals, but clear evidence

170 bserved within lung and kidney grafts during ischemic organ preservation.

171 nts >=80 years, the incidence of the primary ischemic outcome (hazard ratio [HR], 0.97 [95% CI, 0.88-

172 r-old patients, the incidence of the primary ischemic outcome was 17% (HR, 0.83 [95% CI, 0.77-0.89])

173 composite bleeding outcomes and 3 composite ischemic outcomes from randomization through 30 days and

174 ding the temporal and spatial development of ischemic pathophysiology and determining neuronal activi

175 , with colchicine significantly worsening an ischemic phenotype.

176 Furthermore, hindlimb remote ischemic preconditioning induced MCUb expression in the

177 ly minor leukocyte infiltration into acutely ischemic-reperfused cortex and negligible vascular album

178 cardioprotective effects against myocardial ischemic/reperfusion injury, indicating their potential

179 ependent on the excess VEGFA produced by the ischemic retina.

180 iciently suppressed aberrant angiogenesis in ischemic retina.

181 reatment, and bilaterality of the underlying ischemic retinal pathology.

182 s face earlier limb and later cardiovascular ischemic risk that is heightened among patients with pos

183 88], P<0.0001), and for each stroke subtype (ischemic: RR, 0.89 [95% CI, 0.81-0.99], P=0.03; hemorrha

184 imal protection to spinal motor neurons from ischemic spinal cord injury (ISCI).

185 This process was initiated by ischemic spreading depolarizations along with subsequent

186 donor hearts have distinct responses to cold ischemic storage.

187 ajor coronary events (1.64 [1.35, 2.00]) and ischemic stroke (1.87 [1.73, 2.01]).

188 %), with a low incidence of seizures (1.1%), ischemic stroke (1.9%), intracranial hemorrhage (3.5%),

189 we assessed CA status of patients with acute ischemic stroke (AIS) during intravenous r-tPA therapy a

190 son-years; HR, 1.37 [95% CI, 0.88-2.13]) and ischemic stroke (incidence rate, 5.6 versus 3.2 per 1000

191 Several studies have reported a high risk of ischemic stroke (IS) during the acute phase of infective

192 Early discrimination of patients with ischemic stroke (IS) from stroke mimics (SMs) poses a di

193 tcomes including myocardial infarction (MI), ischemic stroke (IS), and peripheral artery disease (PAD

194 th a mild-to-moderate acute noncardioembolic ischemic stroke (NIHSS score <=5) or TIA who were not un

195 and 1.06; and 0.64, 1.75, respectively) and ischemic stroke (odds ratio = 1.74; 95% confidence inter

196 served effect of WHR was mediated by SBP for ischemic stroke (proportion mediated: 12%, 95% CI = 4-20

197 CD (cluster of differentiation)-84 in acute ischemic stroke after recanalization and to dissect the

198 ts was high with 30 days mortality of 31% in ischemic stroke and 42% in intracerebral hemorrhage.

199 In patients with ischemic stroke and atherosclerosis, an LDL-C target of

200 included consecutive patients admitted with ischemic stroke and atrial fibrillation.

201 ortality was 56%, but rates were higher when ischemic stroke and hemorrhagic stroke were present (76%

202 duced sleep slow waves in an animal model of ischemic stroke and identify sleep as a window for posts

203 Summary-level data for ischemic stroke and its subtypes were obtained from the

204 aster thrombolytic treatment times for acute ischemic stroke and modestly lower 1-year all-cause and

205 Secondary outcomes were first subsequent ischemic stroke and the incidence of disability within 3

206 inflammatory response and protected against ischemic stroke by regulating the AIM2 inflammasome.

207 Acute ischemic stroke care provides a useful application to de

208 consortium with 514,791 individuals (60,341 ischemic stroke cases, and 454,450 non-cases).

209 usion prior to endovascular thrombectomy for ischemic stroke compared with alteplase.

210 n is a leading risk factor for dementia, how ischemic stroke contributes to this neurodegenerative co

211 and SRs to be independent prognosticators of ischemic stroke during a median follow-up of 37.6 months

212 as been a cornerstone for treatment of acute ischemic stroke for more than 20 years; however, its use

213 angiography examinations for suspected acute ischemic stroke from February 2017 to June 2018.

214 A) deformations and its prognostic values of ischemic stroke in a large-scale AF population.

215 nt a case of focal cerebral arteriopathy and ischemic stroke in a pediatric patient with coronavirus

216 an intermittent risk factor of bleeding and ischemic stroke in patients with AF.

217 We conclude that RIC in the setting of acute ischemic stroke in rats is safe, reduces infarct size an

218 conventional echocardiographic measures for ischemic stroke in the AF population but not incremental

219 DL-P was consistently associated with MI and ischemic stroke in the overall population.

220 dose in patients with large vessel occlusion ischemic stroke in whom endovascular thrombectomy is pla

221 Secondary prevention of ischemic stroke includes additional carotid surgery or s

222 A specific cohort of suspected acute ischemic stroke is employed and it is found that 99.0% p

223 f intravenous thrombolytic therapy for acute ischemic stroke is time dependent.

224 We applied this framework to an acute ischemic stroke microsimulation model to calculate the d

225 xamine the neuroprotective effects of RIC in ischemic stroke model.

226 luated consecutive patients with cryptogenic ischemic stroke or TIA admitted in a comprehensive strok

227 grelor and aspirin or aspirin alone in acute ischemic stroke or TIA.

228 ion of stroke recurrence after a cryptogenic ischemic stroke or transient ischemic attack (TIA).

229 vessel wall MRI at 7 T in participants with ischemic stroke or transient ischemic attack (TIA).

230 cular events in patients who have had recent ischemic stroke or transient ischemic attack.

231 ns at 7-T MRI in individuals evaluated after ischemic stroke or transient ischemic attack.

232 the 5 trials, a total of 960 subjects had an ischemic stroke over a median follow-up period of 2.5 ye

233 erformed a prespecified post hoc analysis of ischemic stroke patients screened for DWI-fluid-attenuat

234 urrence rate of acute kidney injury in acute ischemic stroke patients was low and was not higher in p

235 We prospectively observed 151 consecutive ischemic stroke patients with embolic large vessel occlu

236 type plasminogen activator; IV tPA) in acute ischemic stroke patients with prior ischemic stroke with

237 orming mechanical thrombectomy (MT) in acute ischemic stroke patients.

238 The underlying etiology of ischemic stroke remains unknown in up to 30% of patients

239 in wild-type mice conferred protection from ischemic stroke to a similar degree as observed in mice

240 g patients aged 65 years or older with acute ischemic stroke who were treated with tissue plasminogen

241 65 years or older who were treated for acute ischemic stroke with intravenous tPA within 4.5 hours fr

242 Individuals with acute ischemic stroke with ipsilateral carotid stenosis of >=5

243 In acute ischemic stroke with unknown time of onset, magnetic res

244 patients treated with IV tPA who had a prior ischemic stroke within 3 months and 30 655 with no histo

245 in acute ischemic stroke patients with prior ischemic stroke within 3 months.

246 (cardiovascular mortality, reinfarction, or ischemic stroke) were examined.

247 ial infarction, 0.94 (95% CI, 0.75-1.18) for ischemic stroke, 0.92 (95% CI, 0.75-1.12) for major blee

248 chemic brain injury, 6% (95% CI, 0.02-0.11%) ischemic stroke, 6% (95% CI, 0.01-0.16%) seizures, and 4

249 = 29-91%) increase in risk for small vessel ischemic stroke, a 197% increase (95% CI = 59-457%) in r

250 val [CI] = 44-113%) in risk for large artery ischemic stroke, a 57% (95% CI = 29-91%) increase in ris

251 Among patients with large vessel occlusion ischemic stroke, a dose of 0.40 mg/kg, compared with 0.2

252 ts, 1.1% (95% CI = 0.8-1.3%, I(2) = 85%) for ischemic stroke, and 0.2% (95% CI = 0.1-0.3%, I(2) = 64%

253 major coronary events, 1.65 [1.50, 1.80] for ischemic stroke, and 1.35 [1.13, 1.61] for hemorrhagic s

254 brillation (AF) is associated with a risk of ischemic stroke, and functional myocardial imaging has o

255 s to be associated with an increased risk of ischemic stroke, and potentially cryptogenic stroke in p

256 emergency interventional treatment of acute ischemic stroke, and treatment in dedicated stroke cente

257 ogic complications: intracranial hemorrhage, ischemic stroke, and/or brain death, as a composite outc

258 A types in patient blood sequenced 2 d after ischemic stroke, comprising massive decreases of microRN

259 r the study outcomes (myocardial infarction, ischemic stroke, heart failure, and cardiovascular morta

260 outcomes including death, all-cause stroke, ischemic stroke, hemorrhagic stroke, and bleeding hospit

261 nd chronic neurological disorders, including ischemic stroke, hemorrhagic stroke, traumatic brain inj

262 ly existing strategy for patients with acute ischemic stroke, however it causes further brain damage

263 bustly associated with increased risk of any ischemic stroke, large artery stroke, and small vessel s

264 tality and hepatic decompensation as well as ischemic stroke, major adverse cardiovascular events, sp

265 mposite of death from cardiovascular causes, ischemic stroke, or myocardial infarction (secondary com

266 eath of CAD, nonfatal myocardial infarction, ischemic stroke, or unstable angina requiring hospitaliz

267 For tPA payments in acute ischemic stroke, our model-based results suggest financi

268 in animal models of congenital deafness and ischemic stroke, revealing that vascular plasticity and

269 ents to the diagnosis and prognosis of acute ischemic stroke, septic shock, lung injuries, insulin re

270 ents with atrial fibrillation (AF) and acute ischemic stroke, the association of prior anticoagulatio

271 ent in many neurological disorders including ischemic stroke, trauma, and chronic neurodegenerative d

272 with edoxaban versus warfarin were seen for ischemic stroke-related hospitalizations in vitamin K an

273 es, such as venous thromboembolism (VTE) and ischemic stroke.

274 of major AF risk factors and higher risk of ischemic stroke.

275 nonsignificant, of myocardial infarction and ischemic stroke.

276 m GRS was a strong, independent predictor of ischemic stroke.

277 nd the predominant cause of heart attack and ischemic stroke.

278 cer cells, and increased brain damage during ischemic stroke.

279 ebral blood flow (CBF) restoration following ischemic stroke.

280 en in 68 (3.5%) of 1,931 patients with acute ischemic stroke.

281 tic strategy to limit brain damage following ischemic stroke.

282 s but poorly understood consequence of acute ischemic stroke.

283 ive effects of lipids and apolipoproteins on ischemic stroke.

284 tiation of pain and neuronal death following ischemic stroke.

285 ribute to the development and progression of ischemic stroke.

286 The clinical end point was ischemic stroke.

287 Ischemic strokes related to atrial fibrillation are high

288 were the only factor associated with recent ischemic symptoms in participants with carotid stenosis.

289 erfusion of greater than 50% of the involved ischemic territory prior to thrombectomy, assessed by co

290 n 30% versus 35%, P < 0.001) but longer cold ischemic time (CIT) (median 21.0 h versus 18.6 h, P < 0.

291 The interaction between ischemic time and alteplase dose was statistically signi

292 16 nautical miles, with an increase in total ischemic time from 3 to 3.4 hours (all P < .001).

293 Ischemic time, defined as the time from symptom onset to

294 y after coronary reperfusion associates with ischemic time.

295 group, donor-recipient size differences, or ischemic time.

296 y, decreasing operative times, and allograft ischemic times, whereas offering protection of implanted

297 tic needs for arterial revascularization and ischemic tissue repair.

298 to recovery of perfusion and preservation of ischemic tissue.

299 Exercise markedly enhanced the ischemic tolerance and the regenerative capacity of fatt

300 tivation of angiogenic functions in the peri-ischemic vasculature.