ライフサイエンスコーパス: ischemia-reperfusion injury

1 cesses: ischemia and subsequent reperfusion (ischemia/reperfusion injury).

2 whereas neon was only explored in myocardial ischemia reperfusion injury.

3 zones of recipient rat hearts 1 month after ischemia reperfusion injury.

4 abbits, and there were too few data on renal ischemia reperfusion injury.

5 ine how selenium distribution is affected by ischemia reperfusion injury.

6 (H2S) production and protection from hepatic ischemia reperfusion injury.

7 ell line cultures using an in vitro model of ischemia reperfusion injury.

8 ed media and delivered to athymic rats after ischemia-reperfusion injury.

9 herapeutic strategy in mitigating myocardial ischemia-reperfusion injury.

10 The pathogenesis of PGD involves ischemia-reperfusion injury.

11 Plexin C1 in a mouse model of early hepatic ischemia-reperfusion injury.

12 ation is restricted by cold preservation and ischemia-reperfusion injury.

13 nd unilateral nephrectomy plus contralateral ischemia-reperfusion injury.

14 evaluate the benefit to patients at risk of ischemia-reperfusion injury.

15 ute coronary occlusion inevitably results in ischemia-reperfusion injury.

16 C1) mice also demonstrated decreased hepatic ischemia-reperfusion injury.

17 y small interfering RNA is effective against ischemia-reperfusion injury.

18 s crucial for reducing the extent of hepatic ischemia-reperfusion injury.

19 -1 (HO-1) degrades heme and protects against ischemia-reperfusion injury.

20 n-mediated activation of integrins for renal ischemia-reperfusion injury.

21 idate the model, we delivered exosomes after ischemia-reperfusion injury.

22 The C1-INH treatment may reduce ischemia-reperfusion injury.

23 al processes in the early and late phases of ischemia-reperfusion injury.

24 to confer protection on heart tissue against ischemia-reperfusion injury.

25 l evidence that CD4(+) T-cells contribute to ischemia-reperfusion injury.

26 ioprotective in all tested models of cardiac ischemia-reperfusion injury.

27 thelial cells and contribute to acute kidney ischemia-reperfusion injury.

28 prevent anticipated therapeutic responses to ischemia-reperfusion injury.

29 s is implicated in the pathogenesis of renal ischemia-reperfusion injury.

30 ive oxygen species (ROS) as a consequence of ischemia-reperfusion injury.

31 sis induced by folic acid (FA) or unilateral ischemia-reperfusion injury.

32 A2A receptor (A2AR) agonism attenuates lung ischemia-reperfusion injury.

33 a major cause of tissue damage during renal ischemia-reperfusion injury.

34 2 activation and protects mice against renal ischemia-reperfusion injury.

35 ) in myeloid cells were protected from renal ischemia-reperfusion injury.

36 tioning effects protecting vital organs from ischemia-reperfusion injury.

37 ations under pathological conditions such as ischemia-reperfusion injury.

38 ch can harness metabolism to robustly combat ischemia-reperfusion injury.

39 inal transplant procedure would cause severe ischemia-reperfusion injury.

40 acute myocardial contractile dysfunction in ischemia-reperfusion injury.

41 regulatory role of IRF3 is relevant to liver ischemia-reperfusion injury.

42 d higher presence of regulatory T cell after ischemia-reperfusion injury.

43 ell (CPC)-derived exosomes in a rat model of ischemia-reperfusion injury.

44 on (tMCAO) model was used to establish brain ischemia-reperfusion injury.

45 inflammatory response after sublethal renal ischemia-reperfusion injury.

46 in mouse models of systemic inflammation and ischemia-reperfusion injury.

47 ated by C1 neurons: protection against renal ischemia-reperfusion injury.

48 the sterile inflammation that follows kidney ischemia-reperfusion injury.

49 s) treatment with necrostatin-1 during renal ischemia-reperfusion injury.

50 at follow intensely loud noise exposures and ischemia-reperfusion injury.

51 quently apoptosis in epithelial cells during ischemia-reperfusion injury.

52 tective effects in models of endotoxemia and ischemia-reperfusion injury.

53 investigated in a rodent model of myocardial ischemia-reperfusion injury.

54 ion of sirtuin 1 is protective after hepatic ischemia-reperfusion injury.

55 o play a significant role in mouse models of ischemia-reperfusion injury.

56 vivo models suggest that C1-INH ameliorates ischemia-reperfusion injury.

57 t of acetaminophen hepatotoxicity or hepatic ischemia-reperfusion injury.

58 ic mechanisms involved in the development of ischemia-reperfusion injury.

59 gated LPS-mediated protection against kidney ischemia/reperfusion injury.

60 g, anti-inflammatory pathways after cerebral ischemia/reperfusion injury.

61 s, and superior renal function 30 days after ischemia/reperfusion injury.

62 of mitochondrial reactive oxygen species in ischemia/reperfusion injury.

63 ked neuroprotective functions after cerebral ischemia/reperfusion injury.

64 eta15-42 (FX06) has been proven to attenuate ischemia/reperfusion injury.

65 AMPK activity is required to protect against ischemia/reperfusion injury.

66 portant pathological mechanism in myocardial ischemia/reperfusion injury.

67 opolysaccharide (LPS) pretreatment on kidney ischemia/reperfusion injury.

68 A4), on the cerebral microcirculation after ischemia/reperfusion injury.

69 ender remote tissues and organs resistant to ischemia/reperfusion injury.

70 ast, present, and future therapies to reduce ischemia/reperfusion injury.

71 ombosis and less inflammatory response after ischemia/reperfusion injury.

72 ificantly alleviated their susceptibility to ischemia/reperfusion injury.

73 which contribute to the pathology of hepatic ischemia/reperfusion injury.

74 perimental models of cerebral and myocardial ischemia/reperfusion injury.

75 d immune cells and contributes to myocardial ischemia/reperfusion injury.

76 limb ischemia/reperfusion reduces myocardial ischemia/reperfusion injury.

77 lso protection from tissue injury in hepatic ischemia/reperfusion injury.

78 agnetic resonance imaging for characterizing ischemia/reperfusion injury.

79 mma2-AMPK sensitizes the heart to myocardial ischemia/reperfusion injury.

80 eurological deficits than sTM after cerebral ischemia/reperfusion injury.

81 ure, electromechanical uncoupling, and acute ischemia/reperfusion injury.

82 nge protein directly activated by cAMP 1) in ischemia/reperfusion injury.

83 the culprit but also a victim of myocardial ischemia/reperfusion injury.

84 a protective effect of these noble gases on ischemia reperfusion injury across a broad range of expe

85 The activity of COX contributes to ischemia-reperfusion injury after intestinal transplanta

86 myocardial necrosis play important roles in ischemia/reperfusion injury after coronary artery occlus

87 and chronic inflammatory diseases, including ischemia/reperfusion injury, allergic asthma, autoimmune

88 ice fully protected the liver against lethal ischemia/reperfusion injury, allowing 100% survival rate

89 Dual molecular imaging of myocardial ischemia/reperfusion injury allows characterization of p

90 Ischemia-reperfusion injury also promoted DC-dependent c

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

92 ysis for argon was only possible in cerebral ischemia reperfusion injury and did not show neuroprotec

93 macologic strategy proposed to prevent renal ischemia-reperfusion injuries and delayed graft function

94 We hypothesized that ischemia-reperfusion injury and antibody-mediated damage

95 from a confluence of processes initiated by ischemia-reperfusion injury and compounded by effector m

96 icrobubble destruction attenuates myocardial ischemia-reperfusion injury and could avoid unwanted sid

97 at the early phase of kidney transplant when ischemia-reperfusion injury and cyclosporin A toxicity m

98 essential role in the early phase of hepatic ischemia-reperfusion injury and determine the extent of

99 been reported to provide protection against ischemia-reperfusion injury and have been safely used in

100 Non-invasive forearm ischemia-reperfusion injury and low flow induced vascula

101 eted hs-MB destruction attenuates myocardial ischemia-reperfusion injury and may avoid unwanted side

102 enic infections but also plays a key role in ischemia-reperfusion injury and other inflammatory disor

103 Tissue necrosis as a consequence of ischemia-reperfusion injury and oxidative damage is a le

104 y pharmacological means ameliorated cerebral ischemia-reperfusion injury and the consequent motor and

105 m outcome after AKI in two models: bilateral ischemia-reperfusion injury and unilateral nephrectomy p

106 s by peritoneal contamination and infection, ischemia-reperfusion-injury and glycerol-induced acute k

107 b ischemia/reperfusion may reduce myocardial ischemia/reperfusion injury and improve patients' progno

108 , whereas suppression of miR-206 exacerbated ischemia/reperfusion injury and prevented pressure overl

109 robust functional recovery after myocardial ischemia/reperfusion injury and significantly reduced my

110 cerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in

111 s such as obesity and type 2 diabetes (T2D), ischemia-reperfusion injury, and neurodegenerative disea

112 etic Plexin C1 in the development of hepatic ischemia-reperfusion injury, and suggest that Plexin C1

113 duces cardiomyocyte (CM) apoptosis, prevents ischemia/reperfusion injury, and improves cardiac functi

114 tment, and/or diagnosis of diabetes, cancer, ischemia/reperfusion injury, and neurodegenerative disea

115 The mechanisms that drive ischemia/reperfusion injury are not well understood; cur

116 d 4) hearts lacking TSPO are as sensitive to ischemia-reperfusion injury as hearts from control mice.

117 and a Semaphorin 7A peptide reduced hepatic ischemia-reperfusion injury, as measured by the levels o

118 stemic iron overload protected against renal ischemia-reperfusion injury-associated sterile inflammat

119 stly, proximal tubule deletion of DRP1 after ischemia-reperfusion injury attenuated progressive kidne

120 to bacterial infection but are resistant to ischemia/reperfusion injury because of defective activat

121 contributors to the acute phase of cerebral ischemia reperfusion injury, but the relevant T cell-der

122 sis, and left ventricular function following ischemia/reperfusion injury, but its role in cardiac arr

123 pan-S1PR agonist, FTY720, attenuates kidney ischemia-reperfusion injury by directly activating S1P1

124 reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation and also

125 Hepatic ischemia-reperfusion injury can result in organ failure,

126 an prevent death by restoring nutrient flow, ischemia/reperfusion injury can cause significant heart

127 ascular diseases, including atherosclerosis, ischemia-reperfusion injury, cardiomyopathy, and heart f

128 variety of pathological disorders including ischemia/reperfusion injury, cataract formation, and neu

129 more, P5779 can protect mice against hepatic ischemia/reperfusion injury, chemical toxicity, and seps

130 as no significant added beneficial effect on ischemia-reperfusion injury compared to propofol.

131 ice demonstrated increased susceptibility to ischemia-reperfusion injury compared with wild-type mice

132 n in vehicle-treated db/db mice subjected to ischemia/reperfusion injury compared with control mice.

133 esthetized mice were subjected to myocardial ischemia reperfusion injury (coronary artery occlusion f

134 c oxide (NO) with positive effects on tissue ischemia/reperfusion injury, cytoprotection, and vasodil

135 This system is especially important in ischemia-reperfusion injury/delayed graft function as we

136 7tg hearts subjected to ischemia or to 24 hr ischemia-reperfusion injury demonstrated significantly l

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

138 ximately 50% 24 h after an in vitro model of ischemia/reperfusion injury, due to delayed fragmentatio

139 Ischemia-reperfusion injury during hepatic resection has

140 le anesthetics such as sevoflurane attenuate ischemia-reperfusion injury during liver resection.

141 ESLD suffer from glycocalyx alterations, and ischemia-reperfusion injury during OLT further exacerbat

142 One month after ischemia/reperfusion injury, EHMs were implanted onto im

143 pathogenesis of inflammatory bowel disease, ischemia-reperfusion injury, enteroinvasive bacterial an

144 experimental studies on donor management and ischemia reperfusion injury focusing on kidney, liver, c

145 tors, cells were irreversibly labeled before ischemia reperfusion injury (genetic cell fate mapping).

146 Three months after ischemia/reperfusion injury, Gottingen swine received tr

147 The extent to which ischemia contributes to ischemia/reperfusion injury has not been thoroughly stud

148 estigated in cerebral, myocardial, and renal ischemia reperfusion injury; helium and xenon have addit

149 results describe a role for Plexin C1 during ischemia-reperfusion injury, highlight the role of hemat

150 get of rapamycin (mTOR) signaling in hepatic ischemia/reperfusion injury (HIRI) in normal and steatot

151 ting the role of epigenetic modifications in ischemia-reperfusion injury, host immune response to the

152 (H2S) is an attractive agent for myocardial ischemia-reperfusion injury, however, systemic delivery

153 SPCs) on the cerebral microcirculation after ischemia-reperfusion injury (I/RI).

154 Delayed graft function (DGF) caused by ischemia/reperfusion injury (I/RI) negatively influences

155 en attributed to organ protective effects in ischemia reperfusion injury in a variety of medical cond

156 been shown to contribute to liver and kidney ischemia reperfusion injury in mice.

157 liorate the damage caused by brain death and ischemia-reperfusion injury in a rat model of kidney and

158 n of small interfering RNA could reduce lung ischemia-reperfusion injury in an ex vivo model reproduc

159 ehydroepiandrosterone protects against renal ischemia-reperfusion injury in male rats.

160 reactive oxygen species (ROS) contributes to ischemia-reperfusion injury in myocardial infarction and

161 onditions such as multiple sclerosis and for ischemia-reperfusion injury in the brain and heart.

162 and L-Cit limits diabetic cardiomyopathy and ischemia/reperfusion injury in db/db mice through a tetr

163 ther with macro- and microscopic evidence of ischemia/reperfusion injury in ileum and colon, but not

164 SEP and L-Cit on diabetic cardiomyopathy and ischemia/reperfusion injury in obese type 2 diabetic mic

165 reduced myocardial infarct size (-63%) after ischemia/reperfusion injury in vivo (all P<0.05).

166 ine kidney lysates, which is elevated during ischemia/reperfusion injury in vivo This induced nuclear

167 but also is critical for the development of ischemia/reperfusion injury in vivo.

168 Macrophages (Mo) are integral in ischemia/reperfusion injury-incited (I/R-incited) acute

169 Renal ischemia-reperfusion injury induced hepatosplenic iron e

170 Ischemia-reperfusion injury induced influx of monocytes,

171 Kidney hypoxia or ischemia-reperfusion injury inevitably occurs during sur

172 by early insults to the allograft, including ischemia/reperfusion injury, infections, and rejection.

173 impaired oxygen supply to the periphery and ischemia reperfusion injury, inflammation, oxidative str

174 Notably, the unavoidable ischemia-reperfusion injury inherent to transplantation

175 flow during organ procurement, and prolonged ischemia-reperfusion injury IRI results in increased rat

176 Ischemia reperfusion injury (IRI) causes tissue and orga

177 s were assessed in hepatic lymphocytes after ischemia reperfusion injury (IRI) in high-fat diet (HFD)

178 Ischemia reperfusion injury (IRI) is one of the major ca

179 identified distinct cellular responses in an ischemia reperfusion injury (IRI) model of AKI.

180 aft survival and correlates with severity of ischemia reperfusion injury (IRI).

181 al role of CD3(+) T cells in mediating early ischemia reperfusion injury (IRI).

182 on and cardiomyocyte injury are hallmarks of ischemia-reperfusion injury (IRI) after heart transplant

183 eatosis is a known risk factor for increased ischemia-reperfusion injury (IRI) and poor outcomes afte

184 modulatory mechanism that protects mice from ischemia-reperfusion injury (IRI) and subsequent AKI.

185 In vivo, more severe renal ischemia-reperfusion injury (IRI) associated with increa

186 he immunologic events surrounding pancreatic ischemia-reperfusion injury (IRI) because of a lack of e

187 les show an improved ability to recover from ischemia-reperfusion injury (IRI) compared with males; h

188 ng the process of tubular repair after renal ischemia-reperfusion injury (IRI) in male Sprague Dawley

189 , and S1P5), and S1PR agonists reduce kidney ischemia-reperfusion injury (IRI) in mice.

190 t regulators CD55 and CD59 exacerbates renal ischemia-reperfusion injury (IRI) in mouse models, but t

191 ctors have been implicated in the process of ischemia-reperfusion injury (IRI) in organ transplantati

192 e of CD47 signaling has been shown to reduce ischemia-reperfusion injury (IRI) in various models of t

193 Ischemia-reperfusion injury (IRI) is a leading cause of

194 Ischemia-reperfusion injury (IRI) is a major cause of AK

195 Ischemia-reperfusion injury (IRI) is an important cause

196 rotection by activated protein C (aPC) after ischemia-reperfusion injury (IRI) is associated with apo

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

198 Ischemia-reperfusion injury (IRI) leading to delayed gra

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

200 hrons expressed few EGFP and RFP puncta, but ischemia-reperfusion injury (IRI) led to dynamic changes

201 modified ultrasound regimen prevents kidney ischemia-reperfusion injury (IRI) likely via the splenic

202 s in lymphoid organs and protected mice from ischemia-reperfusion injury (IRI) more efficiently than

203 e of the CD47 signaling pathway could reduce ischemia-reperfusion injury (IRI) of renal allografts do

204 Liver ischemia-reperfusion injury (IRI) represents a major ris

205 Ischemia-reperfusion injury (IRI) significantly contribu

206 Ischemia-reperfusion injury (IRI) significantly contribu

207 We studied proximal tubules after ischemia-reperfusion injury (IRI) to characterize possib

208 Substantial ischemia-reperfusion injury (IRI) to the transplanted ki

209 of tubular epithelial cell repair following ischemia-reperfusion injury (IRI), a common type of rena

210 Ischemia-reperfusion injury (IRI), an innate immunity-dr

211 Hepatic ischemia-reperfusion injury (IRI), an innate immunity-dr

212 , how this diverse population is affected by ischemia-reperfusion injury (IRI), an obligate part of r

213 o regulated necrosis of parenchymal cells in ischemia-reperfusion injury (IRI), and loss of either Fa

214 le genetic approach in a mouse model of AKI, ischemia-reperfusion injury (IRI), to determine the temp

215 Steatotic livers are more susceptible to ischemia-reperfusion injury (IRI), which is exacerbated

216 ulation of the vagus nerve attenuates kidney ischemia-reperfusion injury (IRI), which promotes the re

217 ific NF-kappaB signaling in a mouse model of ischemia-reperfusion injury (IRI)-induced AKI.

218 C1) stimulation (10 min) protected mice from ischemia-reperfusion injury (IRI).

219 r (TNF)-alpha inhibition was shown to reduce ischemia/reperfusion injury (IRI) after intestinal trans

220 , the pathogenic mechanisms underlying renal ischemia/reperfusion injury (IRI) are not fully defined.

221 s of calorie and protein restriction against ischemia/reperfusion injury (IRI) but also implicate H2S

222 yclonal natural IgM protects mice from renal ischemia/reperfusion injury (IRI) by inhibiting the repe

223 Ischemia/reperfusion injury (IRI) is a central phenomeno

224 To elucidate the role of DAP12 in pulmonary ischemia/reperfusion injury (IRI), we took advantage of

225 c steatosis renders liver more vulnerable to ischemia/reperfusion injury (IRI), which commonly occurs

226 cts of CIAKI in vitro and introduce a murine ischemia/reperfusion injury (IRI)-based approach that al

227 exposed these mice and wild type controls to ischemia/reperfusion injury (IRI).

228 e immune system significantly contributes to ischemia/reperfusion injury (IRI).

229 Hepatic ischemia-reperfusion injury is a disease pattern that is

230 Ischemia-reperfusion injury is exacerbated by the thromb

231 Renal ischemia-reperfusion injury is mediated by a complex cas

232 ndications that the inflammatory response to ischemia-reperfusion injury is mediated by cyclooxygenas

233 circulating proinflammatory cytokines during ischemia-reperfusion injury is not well understood.

234 The etiology of retinal ischemia-reperfusion injury is orchestrated by complex a

235 Ischemia-reperfusion injury is strongly associated with

236 Lung ischemia-reperfusion injury is the main cause of primary

237 Ischemia-reperfusion injury is unavoidably caused by los

238 Ischemia/reperfusion injury is a major cause of acute ki

239 e), in two mouse CKD models, UUO and chronic ischemia reperfusion injury, led to a reduction in fibro

240 ion after occlusion was removed) or hindlimb ischemia reperfusion injury (left leg tourniquet for 90

241 into the infarct border zone 24 hours after ischemia/reperfusion injury, likely owing to reduced tum

242 amniotic fluid stem cells in rats with renal ischemia-reperfusion injury, mainly by mitogenic, angiog

243 nt of THP(-/-) mice with truncated THP after ischemia-reperfusion injury mitigated the worsening of A

244 Results of this study in a renal ischemia-reperfusion injury model allow phenotype and fu

245 fect of amniotic fluid stem cells in a renal ischemia-reperfusion injury model.

246 In a transient cerebral ischemia/reperfusion injury model, Apoe(-/-) mice expres

247 owth factor secretion, and performance in an ischemia/reperfusion injury model.

248 an protective effects mostly in small animal ischemia reperfusion injury models.

249 h cleaves GLP-1, is renoprotective in rodent ischemia-reperfusion injury models.

250 protection in a model of heart damage termed ischemia-reperfusion injury, motivating further study of

251 In this study, we used a renal bilateral ischemia-reperfusion injury mouse model to identify uniq

252 ted to two different models of organ injury: ischemia reperfusion injury of the kidney and cisplatin-

253 herosclerosis and affords protection against ischemia/reperfusion injury of the cerebral cortex.

254 size while improving cardiac function after ischemia/reperfusion injury of the heart.

255 a remote site before a subsequent prolonged ischemia/reperfusion injury of the target organ, is an a

256 use model to investigate the effect of renal ischemia-reperfusion injury on systemic iron homeostasis

257 Low-dose NaNO(2) protects against vascular ischemia-reperfusion injury only when it is given before

258 wn to act as microRNA sponges and to control ischemia-reperfusion injury or act as epigenetic regulat

259 Hepatic ischemia-reperfusion injury or sham operation.

260 plasma samples from rats subjected to renal ischemia-reperfusion injury, pigs subjected to renal tra

261 is associated with various diseases such as ischemia/reperfusion injury, polycystic kidney disease,

262 doxically, it preserves heart function after ischemia/reperfusion injury, potentially by decreasing p

263 ogen and serum creatinine in rats with renal ischemia-reperfusion injury, providing evidence for its

264 In cardiac ischemia-reperfusion injury, reactive oxygen species (RO

265 bred hearts, which are highly susceptible to ischemia-reperfusion injury, recapitulated the early phe

266 -1 (HO-1) expression, which is protective in ischemia-reperfusion injury, regulates trafficking of my

267 Mechanisms of renal ischemia-reperfusion injury remain unresolved, and effec

268 which the Ucn2-CRFR2 axis mitigates against ischemia/reperfusion injury remain incompletely delineat

269 ion of low-potassium dextran (LPD) solution, ischemia-reperfusion injury remains a major contributor

270 Ischemia-reperfusion injury resulted in significantly wo

271 In mouse hearts, ischemia/reperfusion injury resulted in acute JP2 down-r

272 In summary, renal ischemia-reperfusion injury results in profound alterati

273 isolated cells and a mouse model of hepatic ischemia/reperfusion injury revealed that NOX2 from both

274 er, in animal models of peritonitis, hepatic ischemia-reperfusion injury, Salmonella infection, uveit

275 inflammation within the muscle tissue during ischemia/reperfusion injury sensitizes group III and IV

276 In conclusion, in this rat model of ischemia-reperfusion injury, sigma1-receptor agonists im

277 inflammation to mediate protection in renal ischemia-reperfusion injury, suggesting that hepcidin-fe

278 ng pathway can afford protection against the ischemia/reperfusion injury that occurs during myocardia

279 After ischemia-reperfusion injury, THP(-/-) mice, compared wit

280 ndogenous protective mechanism against renal ischemia-reperfusion injury through inhibition of Galpha

281 e to resolve tubular injury after unilateral ischemia-reperfusion injury (U-IRI) led to sustained low

282 Compared with controls, mouse models of ischemia-reperfusion injury, urinary obstruction, and hy

283 We also measured damage after myocardial ischemia reperfusion injury using morphometry, neutrophi

284 tect the heart against subsequent myocardial ischemia/reperfusion injury via direct effects on the my

285 This reduction in ischemia-reperfusion injury was accompanied by reduced n

286 Ischemia-reperfusion injury was induced in lungs isolate

287 Mesenteric ischemia-reperfusion injury was induced in male Wistar r

288 jury in kidneys subjected to bilateral renal ischemia-reperfusion injury was more severe in the absen

289 ntravital microscopy, we found that cerebral ischemia/reperfusion injury was accompanied by neutrophi

290 Ischemia/reperfusion injury was induced in 10-week-old C

291 ogenous selenium administration could reduce ischemia reperfusion injury, we synthesized and administ

292 Using a chimeric mouse model for renal ischemia-reperfusion injury, we found that NLRX1 protect

293 R inhibition with rapamycin protects against ischemia/reperfusion injury, we hypothesized that rapamy

294 tor-amniotic fluid stem cells can worsen the ischemia-reperfusion injury when delivered in a high dos

295 non have additionally been tested in hepatic ischemia reperfusion injury, whereas neon was only explo

296 ced hypertrophy and protected the heart from ischemia/reperfusion injury, whereas suppression of miR-

297 annels renders the heart more susceptible to ischemia/reperfusion injury, whereas the pathological ev

298 portant role of fibrin derivatives in global ischemia/reperfusion injury, which can be attenuated by

299 -)) protects against experimental myocardial ischemia/reperfusion injury with reduced infarct size an

300 osstalk with innate leukocytes in myocardial ischemia-reperfusion injury, wound healing, and remodeli