ライフサイエンスコーパス: reperfusion

1 ligation for 30 minutes followed by 72 hours reperfusion.

2 with lower CBF, likely attributed to earlier reperfusion.

3 rvention strategies to change the outcome of reperfusion.

4 ation, and has a protective role in ischemia reperfusion.

5 ebral artery occlusion (MCAO) and 24-72 h of reperfusion.

6 162S and subjected to simulated ischemia and reperfusion.

7 s coronary intervention, fibrinolysis, or no reperfusion.

8 -treated organs had greater and more uniform reperfusion.

9 nd SNRK reduces infarct size after ischaemia/reperfusion.

10 e adhesion and emigration following ischemia-reperfusion.

11 isphere middle-cerebral artery occlusion and reperfusion.

12 l of liver partial warm ischemia and in situ reperfusion.

13 pening and damages the heart during ischemia/reperfusion.

14 n, acute kidney injury, and cardiac ischemia/reperfusion.

15 rotective effects of CDCs administered after reperfusion.

16 Hepatic hemodynamics were recorded after reperfusion.

17 meability transition pores (PTP) open during reperfusion.

18 ed in greater cardiac injury during ischemia-reperfusion.

19 art reduced soluble MER levels post-ischemia reperfusion.

20 the flow, the shorter the time for efficient reperfusion.

21 l uncoupling, and protects against ischaemia/reperfusion.

22 lar oxidant production during liver ischemia-reperfusion.

23 , isolated hearts were subjected to ischemia/reperfusion.

24 tly after onset of ischemia and during blood reperfusion.

25 in cardiac repair after myocardial ischemia reperfusion.

26 cruited phagocytes after myocardial ischemia reperfusion.

27 of the cell's condition up to the moment of reperfusion.

28 clusion (MCAO) and sacrificed at 24 hours of reperfusion.

29 , resulted in more patients receiving timely reperfusion.

30 ns at 120 minutes and 1, 4, and 7 days after reperfusion.

31 ction as thrombolysis patients with complete reperfusion.

32 s the survival of the myocardium at ischemia/reperfusion.

33 ar effectors in the CNS response to ischemia/reperfusion.

34 manent ligation, 1280.0+/-162.6 ms; ischemia/reperfusion, 1115.0+/-140.5 ms; P<0.001; n=14/13), which

35 At early reperfusion (120 min), the ischemic area showed a coordi

36 1: permanent ligation, 24.5+/-7.0%; ischemia/reperfusion, 33.7+/-11.6%; P<0.05; n=14/13).

37 29 versus 127), and were with longer time to reperfusion (42 minutes longer).

38 For patients who achieve rapid reperfusion, a stricter rCBF threshold to estimate the i

39 ained significantly impaired after 10 min of reperfusion after global ischemia.

40 the enzyme SENP3 promotes cell death during reperfusion after ischaemia by enhancing Drp1 partitioni

41 ischemic muscles to allow sufficient tissue reperfusion after ischemic injury.

42 RATIONALE: Clinical benefits of reperfusion after myocardial infarction are offset by ma

43 S AND In humans, we discovered that clinical reperfusion after myocardial infarction led to significa

44 tPA-induced brain hemisphere reperfusion after photothrombolic middle cerebral artery

45 ischemic stroke patients with known complete reperfusion after thrombectomy had the same baseline com

46 on the kidney, we used a bilateral ischemia-reperfusion AKI mouse model, in which gallein attenuated

47 Because prolonged ischemia/reperfusion also damages electron transport complexes, w

48 Reperfusion alters post-myocardial infarction (MI) heali

49 e potential mediators in both acute ischemia/reperfusion and adaptations to chronic ischemic conditio

50 rtal venous reperfusion and hepatic arterial reperfusion and analyzed by liquid chromatography-mass s

51 k-old Wistar rats were subjected to ischemia-reperfusion and assigned to four groups: amniotic fluid

52 ally scanned (within the first 3 hours after reperfusion and at 1, 4, 7, and 40 days), and controls w

53 T cells to cardiac remodeling after ischemia/reperfusion and define its mechanism of action.

54 initial work-up of chest pain and early post-reperfusion and follow-up evaluation of ACS to identify

55 The robust association between endovascular reperfusion and good outcome among patients with the CT

56 n, as well as 30 minutes after portal venous reperfusion and hepatic arterial reperfusion and analyze

57 ls of acute liver damage induced by ischemia reperfusion and N-acetyl-p-aminophenol (acetaminophen) a

58 To examine access to reperfusion and percutaneous coronary intervention (PCI)

59 of adenine nucleotides change rapidly after reperfusion and ratios of ATP/ADP/AMP after reperfusion

60 d to suppress pre-rRNA level during ischemia/reperfusion and showed a greater infarct size.

61 tinal injury occurs during ischemia prior to reperfusion and that this is due to activation of C3 wit

62 Myocardial responses to acute ischemia/reperfusion and to chronic ischemic conditions have been

63 ECGs were collected at baseline, after reperfusion, and analyzed for the presence of Q waves us

64 n of patients undergoing reperfusion, timely reperfusion, and postfibrinolysis angiography and PCI.

65 reperfusion and ratios of ATP/ADP/AMP after reperfusion are significantly correlated to graft functi

66 ry injury induced by intestinal ischemia and reperfusion, as well as in a model of lung infection by

67 nt myocardial infarction induced by ischemia/reperfusion before intracoronary infusion of CDCexo, ine

68 lusion of a rat coronary artery, followed by reperfusion, blocks 40% of cardiac capillaries and halve

69 inhalational anesthetics can reduce ischemia-reperfusion brain injury, although the cellular mechanis

70 transplant group was more likely to receive reperfusion compared with the stage 5D CKD group (adjust

71 size and LV macrophage content after 24-48 h reperfusion compared with wildtype (WT) counterparts.

72 ator-1 Project, we hypothesized that time to reperfusion could be further reduced with enhanced regio

73 strate that TASK channels can limit ischemia-reperfusion damage in the cortex, and postconditioning w

74 was increased upon endotoxemia and ischemia reperfusion damage where CB2 receptors play a protective

75 renal signaling processes increased at later reperfusion (day 4 and 7).

76 Type of reperfusion did not modify the association of baseline Q

77 the pathological events elicited by ischemia/reperfusion do not involve BK in vascular smooth muscle

78 e that incorporates donor, preservation, and reperfusion factors.

79 To this end, after 4 weeks of reperfusion, fibrotic tissue increased and myocardial st

80 study, 20 pigs underwent 40-minute ischemia/reperfusion followed by serial CMR examinations at 120 m

81 l review board protocol 2 hours after portal reperfusion, followed by Western blot analyses.

82 ed to 45 min of coronary artery ligation and reperfusion for 12 weeks.

83 mesenteric artery for 90 min and subsequent reperfusion for 120 min.

84 minutes of warm hepatic ischemia followed by reperfusion for 6 or 24 hours.

85 warm renal ischemia, and analyzed 24 h after reperfusion for renal function (serum creatinine and ure

86 therapy offers an alternative to mechanical reperfusion for ST-segment elevation myocardial infarcti

87 renal transplant group received in-hospital reperfusion for STEMI.

88 Successful reperfusion, functional independence (modified Rankin Sc

89 The number of passes, rate of successful reperfusion, functional independence at 90 days, mortali

90 ure with MAC had similar rates of successful reperfusion, good clinical outcomes, hemorrhagic complic

91 erts a protective effect in hepatic ischemia-reperfusion (HIR) injury.

92 After reperfusion, HMP-preserved livers functioned better and

93 For reperfusion, hospitals were grouped by whether a specifi

94 sis enhances hepatic sensitivity to ischemia reperfusion (I/R) and impedes liver regeneration (LR).

95 plays a protective role in cardiac ischemia/reperfusion (I/R) but the molecular mechanism remains un

96 ATF6-mediated ER stress response on ischemia/reperfusion (I/R) in cardiac myocytes and mouse hearts.

97 rum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice.

98 Intestinal ischemia/reperfusion (I/R) injury is a relatively common patholog

99 Cerebral ischemia/reperfusion (I/R) injury, expression of adhesion molecul

100 kidney are innately susceptible to ischemia-reperfusion (I/R) injury, which can originate from sourc

101 ion-each initiated after myocardial ischemia-reperfusion (I/R) injury-was investigated to evaluate th

102 tudied its expression in mesenteric ischemia-reperfusion (I/R) injury.

103 ffects were examined in mouse focal ischemia/reperfusion (I/R) model.

104 tegies and ischemia duration on postischemia/reperfusion (I/R) myocardial tissue composition (edema,

105 nvestigated the role of TRAF3IP2 in ischemia/reperfusion (I/R)-induced nitroxidative stress, inflamma

106 e early molecular changes following ischemia/reperfusion (I/R).

107 e aminotransferase (ALT) (marker of ischemia-reperfusion [I/R] injury) were measured in perfusion flu

108 balloon occlusions followed by 30 seconds of reperfusion immediately after opening of the infarct-rel

109 ed infarct size declined progressively after reperfusion in all groups.

110 esponse within microglia exposed to ischemia/reperfusion in both in vitro and in vivo experimental pa

111 iated with significant reductions in time to reperfusion in patients with ST-segment-elevation myocar

112 amaged mucosa induced by mesenteric ischemia/reperfusion in the small intestine and by dextran sulfat

113 on and fibrinolysis, as may occur upon graft reperfusion in vivo.

114 transplant recipients with STEMI, the use of reperfusion increased from 53.7% in the 2003-2004 interv

115 At the time of reperfusion, indocyanine green-based in vivo imaging sho

116 tion and higher sensitivity to ischemia- and reperfusion- induced injury).

117 interferon (IFN) signaling in both ischemia/reperfusion-induced brain injury and ischemic preconditi

118 for the recently-discovered role of NAADP in reperfusion-induced cell death.

119 mTOR activation protects liver from ischemia/reperfusion-induced injury through NF-kappaB pathway.

120 eletion of Drp1 prevented the renal ischemia-reperfusion-induced kidney injury, inflammation, and pro

121 both in vitro H/H-N/N- and in vivo ischemia/reperfusion-induced microglial ISG responses by quantita

122 Together, these data suggest novel ischemia/reperfusion-induced pathways for both TLR4-dependent and

123 sinated eIF5A and protected against ischemia-reperfusion-induced renal injury.

124 pamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and steatotic liver

125 the cerebral microcirculation after ischemia-reperfusion injury (I/RI).

126 hogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined.

127 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with increased expre

128 sessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in high-fat diet (HFD)-fed mice

129 ors CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but the effect

130 signaling has been shown to reduce ischemia-reperfusion injury (IRI) in various models of tissue isc

131 Ischemia-reperfusion injury (IRI) is a leading cause of AKI.

132 Ischemia-reperfusion injury (IRI) is an important cause of acute

133 Ischemia and reperfusion injury (IRI) is an inevitable event in conve

134 by activated protein C (aPC) after ischemia-reperfusion injury (IRI) is associated with apoptosis in

135 However, its role in renal ischemia-reperfusion injury (IRI) is controversial.

136 Ischemia-reperfusion injury (IRI) leading to delayed graft functi

137 Renal ischemia-reperfusion injury (IRI) leads to acute kidney injury an

138 hoid organs and protected mice from ischemia-reperfusion injury (IRI) more efficiently than either cy

139 CD47 signaling pathway could reduce ischemia-reperfusion injury (IRI) of renal allografts donated aft

140 Liver ischemia-reperfusion injury (IRI) represents a major risk factor

141 ar epithelial cell repair following ischemia-reperfusion injury (IRI), a common type of renal stresso

142 s diverse population is affected by ischemia-reperfusion injury (IRI), an obligate part of renal tran

143 is renders liver more vulnerable to ischemia/reperfusion injury (IRI), which commonly occurs in trans

144 lation (10 min) protected mice from ischemia-reperfusion injury (IRI).

145 Post-ischemic reperfusion injury (PIRI) triggers an intense inflammato

146 lve tubular injury after unilateral ischemia-reperfusion injury (U-IRI) led to sustained low-level Ch

147 ing reactive oxygen species (ROS) underlying reperfusion injury after prolonged cardiac ischemia.

148 Ischemia-reperfusion injury also promoted DC-dependent cross-pres

149 rly phase of kidney transplant when ischemia-reperfusion injury and cyclosporin A toxicity may coexis

150 a/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' prognosis after

151 ological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and neurolog

152 e subjected to ex vivo reperfusion, modeling reperfusion injury and were similarly analyzed for energ

153 ximal tubule deletion of DRP1 after ischemia-reperfusion injury attenuated progressive kidney injury

154 ents age-related intolerance to ischemia and reperfusion injury by modulating substrate metabolism.

155 an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also provides

156 Here, we demonstrate that metoprolol reduces reperfusion injury by targeting the haematopoietic compa

157 renal function, possibly because of ischemia/reperfusion injury developing after PTRA.

158 Ischemia-reperfusion injury during hepatic resection has been sho

159 nt to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly studied.

160 androsterone protects against renal ischemia-reperfusion injury in male rats.

161 Ischemia-reperfusion injury induced influx of monocytes, DCs, mac

162 Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation is mediat

163 ng organ procurement, and prolonged ischemia-reperfusion injury IRI results in increased rates of del

164 Reperfusion injury is largely attributed to excess mitoc

165 ng proinflammatory cytokines during ischemia-reperfusion injury is not well understood.

166 Ischemia-reperfusion injury is unavoidably caused by loss and sub

167 is key to improving outcomes, yet consequent reperfusion injury may be harmful.

168 (-/-) mice with truncated THP after ischemia-reperfusion injury mitigated the worsening of AKI.

169 mniotic fluid stem cells in a renal ischemia-reperfusion injury model.

170 osis and affords protection against ischemia/reperfusion injury of the cerebral cortex.

171 Severe ischaemia-reperfusion injury of the right kidney, with subsequent

172 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effective ther

173 y can afford protection against the ischemia/reperfusion injury that occurs during myocardial infarct

174 Mesenteric ischemia-reperfusion injury was induced in male Wistar rats (six

175 tic fluid stem cells can worsen the ischemia-reperfusion injury when delivered in a high dose.

176 cts against experimental myocardial ischemia/reperfusion injury with reduced infarct size and cardiom

177 ic inflammatory diseases, including ischemia/reperfusion injury, allergic asthma, autoimmune nephriti

178 protected the liver against lethal ischemia/reperfusion injury, allowing 100% survival rate.

179 Six hours after induction of renal ischemia-reperfusion injury, amniotic fluid stem cells, vascular

180 diomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac function in isc

181 hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in mammals a

182 obesity and type 2 diabetes (T2D), ischemia-reperfusion injury, and neurodegenerative diseases.

183 of pathological disorders including ischemia/reperfusion injury, cataract formation, and neurodegener

184 een extensively used to investigate ischemic-reperfusion injury, immunological consequences during he

185 insults to the allograft, including ischemia/reperfusion injury, infections, and rejection.

186 oxygen supply to the periphery and ischemia reperfusion injury, inflammation, oxidative stress, and

187 fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic, angiogenic, and

188 amples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to renal transplantat

189 , it preserves heart function after ischemia/reperfusion injury, potentially by decreasing proteolysi

190 In conclusion, in this rat model of ischemia-reperfusion injury, sigma1-receptor agonists improved po

191 After ischemia-reperfusion injury, THP(-/-) mice, compared with wild-ty

192 ared with controls, mouse models of ischemia-reperfusion injury, urinary obstruction, and hypertensio

193 ng a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protects against

194 nders the heart more susceptible to ischemia/reperfusion injury, whereas the pathological events elic

195 on overload protected against renal ischemia-reperfusion injury-associated sterile inflammation.

196 emia/reperfusion reduces myocardial ischemia/reperfusion injury.

197 sensitizes the heart to myocardial ischemia/reperfusion injury.

198 ent with necrostatin-1 during renal ischemia-reperfusion injury.

199 -derived exosomes in a rat model of ischemia-reperfusion injury.

200 times and to ameliorate the consequences of reperfusion injury.

201 ) model was used to establish brain ischemia-reperfusion injury.

202 tory response after sublethal renal ischemia-reperfusion injury.

203 poptosis in epithelial cells during ischemia-reperfusion injury.

204 al deficits than sTM after cerebral ischemia/reperfusion injury.

205 models of systemic inflammation and ischemia-reperfusion injury.

206 1 neurons: protection against renal ischemia-reperfusion injury.

207 cultures using an in vitro model of ischemia reperfusion injury.

208 tromechanical uncoupling, and acute ischemia/reperfusion injury.

209 le inflammation that follows kidney ischemia-reperfusion injury.

210 intensely loud noise exposures and ischemia-reperfusion injury.

211 ffects in models of endotoxemia and ischemia-reperfusion injury.

212 novel contributor and therapeutic target of reperfusion injury.

213 this compound as a novel adjunct therapy for reperfusion injury.

214 and delivered to athymic rats after ischemia-reperfusion injury.

215 vity is required to protect against ischemia/reperfusion injury.

216 presence of regulatory T cell after ischemia-reperfusion injury.

217 ed by folic acid (FA) or unilateral ischemia-reperfusion injury.

218 recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardiomyocytes are a known

219 toneal contamination and infection, ischemia-reperfusion-injury and glycerol-induced acute kidney-inj

220 ocellular injury when exposed to an ischemic-reperfusion insult.

221 Retinal ischemia-reperfusion (IR) injury causes irreversible loss of neur

222 Hepatic ischemia-reperfusion (IR) injury is a common clinical issue lacki

223 re crucial early effectors in organ ischemia-reperfusion (IR) injury.

224 ly demonstrated in a swine model of ischemia-reperfusion (IR) that hypercholesterolemia abolishes HDL

225 antagonism prevents AKI induced by ischemia-reperfusion (IR).

226 Renal ischemia/reperfusion is a major cause of acute kidney injury.

227 r by how much the time window for successful reperfusion is extended by preconditioning, and how long

228 xplanation may be incomplete, because RET on reperfusion is self-limiting and therefore transient.

229 e cryopreservation and auto-transplantation, reperfusion ischemia and hypoxia have been reported as m

230 nding coronary artery occlusion, followed by reperfusion (ischemia-reperfusion MI).

231 Intestinal ischemia followed by reperfusion leads to local and remote organ injury attri

232 To determine the effects of "ischemia/reperfusion-like" conditions on microglia, we performed

233 stration of cardiosphere-derived cells after reperfusion limits infarct size measured acutely, while

234 e efflux from the matrix, PTP opening during reperfusion may activate sustained ROS production by thi

235 a viability test in combination with ex vivo reperfusion may provide a useful predictor of outcome th

236 C) by repeated brief cycles of limb ischemia/reperfusion may reduce myocardial ischemia/reperfusion i

237 occlusion, followed by reperfusion (ischemia-reperfusion MI).

238 cts in a murine model of myocardial ischemia-reperfusion (MI/R) injury with a bell shape therapeutic

239 mal1(fx/fx);Tek-Cre mice, a retinal ischemia/reperfusion model and a neointimal hyperplasia model of

240 In the simulated reperfusion model, a similar trend in adenine nucleotide

241 sing a middle cerebral artery occlusion with reperfusion model.

242 regenerative procedures follows an ischemia-reperfusion model.

243 atory death livers were subjected to ex vivo reperfusion, modeling reperfusion injury and were simila

244 at 120 min, 24 hours, 4days, and 7days after reperfusion (n = 5 per group).

245 rtery ligation (n=14) or 50 minutes ischemia/reperfusion (n=13).

246 only treatment with proven efficacy is early reperfusion of the occluded coronary artery.

247 impaired in aged hearts during ischemia and reperfusion (P < 0.05 vs. young hearts).

248 tochondrial Zn(2+) accumulation in the early reperfusion period may be a critical and targetable upst

249 tributed to inflammatory response during the reperfusion phase.

250 lung water may prove valuable for diagnosing reperfusion pulmonary edema after pulmonary endarterecto

251 Overall, 26 patients (84%) experienced reperfusion pulmonary edema during the first 72 hours af

252 Reperfusion pulmonary edema is a specific complication o

253 ry endarterectomy is closely associated with reperfusion pulmonary edema occurrence in the next 48 ho

254 r measurement may be valuable for diagnosing reperfusion pulmonary edema.

255 e myocardial areas after repetitive ischemia/reperfusion (r-I/R) injury without ensuing myocardial in

256 To compare in-hospital reperfusion rates and outcomes of ST-segment elevation M

257 Administration of CDCexo but not Fbexo after reperfusion reduces infarct size in rat and pig models o

258 C) by repeated brief cycles of limb ischemia/reperfusion reduces myocardial ischemia/reperfusion inju

259 TP:AMP and energy charge after portal venous reperfusion, respectively.

260 Paradoxically, reperfusion results in nitroxidative stress and a marked

261 Given intravenously at reperfusion/resuscitation to rats, ATTM significantly re

262 A systems approach using ECLS and reperfusion seemed to improve functionally favorable sur

263 At 4 weeks post-reperfusion, SHR and WKY underwent either bilateral RF-R

264 unct cardioprotection by postconditioning at reperfusion still protects.

265 farction, focusing on the recent advances in reperfusion strategies and pharmacological treatment app

266 events in real-world patients, regardless of reperfusion strategy used.

267 seline Q waves, time from symptom onset, and reperfusion strategy with in-hospital clinical outcomes.

268 important in the pathophysiology of ischemia/reperfusion (stroke)-induced injury and recovery.

269 rovascular obstruction (MVO) are markers for reperfusion success.

270 The recipient did not suffer post-reperfusion syndrome or vasoplegia after revascularizati

271 l cord injury after thoracic aortic ischemia-reperfusion (TAR) in mice.

272 er, these differences diminished by 2011 for reperfusion therapy (54% in urban versus 57% in rural; P

273 rials that compared fibrinolytic agents as a reperfusion therapy in adult patients with STEMI, whethe

274 gating agents with an approved indication of reperfusion therapy in STEMI (streptokinase, tenecteplas

275 exist among various fibrinolytic regimens as reperfusion therapy in STEMI and alteplase (accelerated

276 y gain was found in patients with STEMI with reperfusion therapy or in patients with NSTEMI, whether

277 We tested the hypotheses that reperfusion therapy with tenecteplase would be superior

278 tability or ongoing ischemic symptoms, prior reperfusion therapy, risk level as assessed by noninvasi

279 ed after 2010 in patients with STEMI without reperfusion therapy, whereas no further mortality gain w

280 sed on the proportion of patients undergoing reperfusion, timely reperfusion, and postfibrinolysis an

281 Regional variations in reperfusion times and mortality in patients with ST-segm

282 dium declines significantly from early after reperfusion to 24 hours, and then increases up to day 4,

283 periments on cardioprotection beyond that by reperfusion to clinical practice has to date been disapp

284 expansion and thus could still benefit from reperfusion to reduce their degree of disability.

285 Overall reperfusion use and times to reperfusion were similar (7

286 Tissue damage associated with ischemia-reperfusion, vascular injury, and/or rejection creates p

287 50% reduction of infarct size after ischemia/reperfusion versus wild type.

288 Rate of reperfusion was 89%.

289 In patients with target mismatch (n = 131), reperfusion was associated with higher odds of favorable

290 Reperfusion was defined as >50% reduction in critical hy

291 Myocardial ischemia (50 minutes followed by reperfusion) was induced in global CD73(-/-) and CD4-CD7

292 e mice treated with rhCD55 immediately after reperfusion were also protected in the moderate IRI mode

293 Overall reperfusion use and times to reperfusion were similar (795 [88.5%] vs 1372 [90.1%]; P

294 Baseline Q waves, but not time to reperfusion, were associated with an increased odds of t

295 ions did not reconstitute AKI after ischemia-reperfusion, whereas macrophages cultured in physiologic

296 ins was different between baseline and early reperfusion with RIPC and/or with sham.

297 d higher expression/phosphorylation at early reperfusion with RIPC in comparison to sham revealed a r

298 rostaglandin reductase 2 expression at early reperfusion with RIPC than with sham in patients.

299 nucleotides was observed following clinical reperfusion, with a 2.45-, 3.17- and 2.12-fold increase

300 and from pigs undergoing coronary occlusion/reperfusion without (sham) and with RIPC.