ライフサイエンスコーパス: ischaemia

1 the central nervous system during myocardial ischaemia.

2 ould be a therapeutic target in white matter ischaemia.

3 TRPA1 block reduces myelin damage in ischaemia.

4 yte viability under starvation and simulated ischaemia.

5 ccumulation with better renal function after ischaemia.

6 y elevated extracellular K(+), decoupling or ischaemia.

7 ccur only in pathological conditions such as ischaemia.

8 y render the kidney especially vulnerable to ischaemia.

9 naptic terminals in the early phase of brain ischaemia.

10 of atherosclerosis in relation to myocardial ischaemia.

11 naptic terminals in the early phase of brain ischaemia.

12 rce about their ability to reduce angina and ischaemia.

13 Rs are dependent on ASIC1a activation during ischaemia.

14 ss in the presence and absence of myocardial ischaemia.

15 res at presynaptic terminals during in vitro ischaemia.

16 is defective, resulting in functional muscle ischaemia.

17 flammation and subsequent brain damage after ischaemia.

18 cardiography to detect or exclude myocardial ischaemia.

19 sis as a complication of random-pattern flap ischaemia.

20 +)/c-Kit(+) cells in mice following hindlimb ischaemia.

21 ue correlates with the degree of ante-mortem ischaemia.

22 aired functional recovery following hindlimb ischaemia.

23 is protective in a mouse model of myocardial ischaemia.

24 d inotrope use during the 48 h after hypoxia-ischaemia.

25 FCCP, was observed between 27 and 69 min of ischaemia.

26 ecreased in the cortex at 48 h after hypoxia-ischaemia.

27 culature, resulting in end-organ optic nerve ischaemia.

28 ity and brain infarction in mice after focal ischaemia.

29 naive rats and animals subjected to cerebral ischaemia.

30 rt and vasculature from oxidative stress and ischaemia.

31 thin C-fibres of DRG neurons after hindlimb ischaemia.

32 eld rapid flow restoration in acute cerebral ischaemia.

33 eutic potential in a mouse model of cerebral ischaemia.

34 after circulatory death with prolonged warm ischaemia.

35 ring endovascular treatment of critical limb ischaemia.

36 ring endovascular treatment of critical limb ischaemia.

37 and protects mice from prolonged myocardial ischaemia.

38 urs in pathological states including cardiac ischaemia.

39 01-in mouse and rat models of focal cerebral ischaemia.

40 schaemia and during 20 min of recovery after ischaemia.

41 essel disease to confirm or exclude balanced ischaemia.

42 ation in the ischaemic territory 1 day after ischaemia.

43 ed blood-brain barrier damage after cerebral ischaemia.

44 lity as a stand-alone marker for acute brain ischaemia.

45 rrent events in patients with acute cerebral ischaemia.

46 0 (19 [1%] vs 21 [1%]) had grade 3-5 cardiac ischaemia.

47 bs using two murine models of injury-induced ischaemia.

48 store depleted energy stores during cerebral ischaemia.

49 AMPAR subunit composition in the response to ischaemia.

50 ole group) had grade 3-5 CNS cerebrovascular ischaemia, 16 (nine [<1%] vs seven [<1%]) had grade 3-5

51 inephrectomy (UNX) and 35 min of left kidney ischaemia-24 h reperfusion, IR).

52 IMD 1 nmol l(-)(1) present throughout ischaemia (3 h) and reperfusion (1 h) attenuated injury

53 During ischaemia, a dramatic decrease in MPA, reaching the low/

54 After cardiac ischaemia, a prolonged decrease of coronary microvascula

55 The association of early ischaemia, admission clinical status, risk factors and 3

56 bit cardiomyocytes were exposed to simulated ischaemia after incubation in the presence of normal (5

57 dorff preparation were exposed to IR (30 min ischaemia) after 4 treatments administered randomly, all

58 but the challenge of balancing the risks of ischaemia and bleeding remains substantial.

59 essed at rest, during 30 min of induced limb ischaemia and during 20 min of recovery after ischaemia.

60 or the non-invasive evaluation of myocardial ischaemia and enables the recording of heart rate variab

61 they sense metabolic changes associated with ischaemia and exercise, and contribute to the metabolic

62 GPBB demonstrates robust response to acute ischaemia and high sensitivity for small infarcts.

63 ti-inflammatory drug (NSAID) alleviates this ischaemia and improves the murine dystrophic phenotype.

64 These findings in cardiac ischaemia and in neuroblastoma suggest that TRPM2 has a

65 the most effective ways to limit myocardial ischaemia and infarct size and thereby reduce the risk o

66 d this vaso-occlusion leads to distal tissue ischaemia and inflammation, with symptoms defining the a

67 be responsible for promoting dementia after ischaemia and mCRP clearance could inform therapeutic av

68 aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesions in diffe

69 aged 18-85 years with evidence of myocardial ischaemia and one or two de-novo native lesions in diffe

70 ute a new cell therapy for treating cerebral ischaemia and other neurological diseases.

71 Documentation of ischaemia and plaque burden is fundamental in the risk s

72 Acute myocardial ischaemia and reperfusion (I-R) are major causes of vent

73 Remote ischaemic conditioning with transient ischaemia and reperfusion applied to the arm has been sh

74 chaemic conditioning treatment (intermittent ischaemia and reperfusion applied to the arm through fou

75 ling can promote chronic inflammation during ischaemia and reperfusion injury, inflammatory bowel dis

76 Remote ischaemic preconditioning uses brief ischaemia and reperfusion of a distant organ to protect

77 a conserved metabolic response of tissues to ischaemia and reperfusion that unifies many hitherto unc

78 ide (H(2)O(2), 1 mmol l(-)(1)) and simulated ischaemia and reperfusion were investigated using recept

79 nd neovessels de novo in a hindlimb model of ischaemia and resulted in a 50% increase in perfusion co

80 However, control Doppler US disclosed no ischaemia and successful exclusion of the aneurysm.

81 In models of both injury ischaemia and tumor angiogenesis, we find that Apln-CreE

82 eficient angiogenesis in models of hind limb ischaemia and tumour-implant growth.

83 urs, similar to non-haemorrhagic necrosis in ischaemia and unlike haemorrhagic necrosis induced by tu

84 logical status after SAH and predicts future ischaemia and worse functional outcomes.

85 a, which are characterized by uteroplacental ischaemia and/or fetal hypoxia.

86 cy disorders characterized by uteroplacental ischaemia and/or fetal hypoxia.

87 or thoracic aorta; (4) transient ventricular ischaemia, and (5) neurally induced AF.

88 able or unstable angina or documented silent ischaemia, and a maximum of two de-novo lesions with a r

89 sion increased sensitivity to focal cerebral ischaemia, and blocking of cortical spreading depression

90 palmar-plantar erythrodysesthesia, cerebral ischaemia, and deep-vein thrombosis.

91 cardiomyopathies, heart failure, myocardial ischaemia, and hypertrophy.

92 ppears a promising therapy for short-lasting ischaemia, and is attractive clinically as it could be s

93 attribute subendocardial fibrosis in POH to ischaemia, and reduced fibrosis in VOH to collagen degra

94 g was retained following chronic distributed ischaemia, and that the impact of capillary rarefaction

95 se sympathetic nerve fibres are sensitive to ischaemia, and that VRCs provide a method to study chang

96 d to the extent of damage following cerebral ischaemia, and the targeting of this inflammation has em

97 esponse, cerebrovascular autoregulation, and ischaemia are critical processes to monitor and target t

98 intracranial artery dissection and cerebral ischaemia are treated with antithrombotics.

99 s that stimulates renal vasoconstriction and ischaemia as a consequence of the physiological redistri

100 vidence of ipsilateral haemodynamic cerebral ischaemia as measured by PET OEF, while 50 (64.9%) had n

101 copy were acquired before and during hypoxia-ischaemia, at 24 and 48 h after resuscitation.

102 y used test for the assessment of myocardial ischaemia, but its diagnostic accuracy is reported to be

103 promotes cell death during reperfusion after ischaemia by enhancing Drp1 partitioning to the mitochon

104 rat hearts were subjected to acute regional ischaemia by ligation of the left anterior descending ar

105 irst 24 h following transient focal cerebral ischaemia by using mice with each isoform genetically su

106 pathophysiological parameters of myocardial ischaemia can be achieved.

107 KEY POINTS: Chronic limb ischaemia, characterized by inflammatory mediator releas

108 ed model of brain injury induced by cerebral ischaemia combined with fast in vivo two-photon calcium

109 ain imaging signs of brain frailty and acute ischaemia contribute to the prognosis of thrombolysis-tr

110 ed as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal subarachno

111 clinical/radiological cVSP, delayed cerebral ischaemia (DCI), and 3-month functional outcomes.

112 es and reduce microvascular blood flow after ischaemia, despite re-opening of the culprit artery.

113 Viabilities under 6 h simulated ischaemia differed (P<0.05) in the absence and presence

114 In the absence of myocardial ischaemia, dobutamine stress is associated with a residu

115 nd bevacizumab group), and visceral arterial ischaemia (docetaxel followed by doxorubicin plus cyclop

116 ce of ischaemia-driven revascularisation and ischaemia-driven hospitalisation did not differ signific

117 nce of ischaemia-driven revascularisation or ischaemia-driven hospitalisation without revascularisati

118 tion (1.12, 1.03-1.23) and seemingly also by ischaemia-driven revascularisation (1.16, 0.997-1.34) wi

119 Incidence of ischaemia-driven revascularisation and ischaemia-driven

120 (all-cause death, myocardial infarction, or ischaemia-driven revascularisation at 48 h) by 19% (3.6%

121 olazine did not reduce the composite rate of ischaemia-driven revascularisation or hospitalisation wi

122 ary endpoint was time to first occurrence of ischaemia-driven revascularisation or ischaemia-driven h

123 endpoints were death, myocardial infarction, ischaemia-driven revascularisation, and stent thrombosis

124 y composite of death, myocardial infarction, ischaemia-driven revascularisation, or stent thrombosis

125 ]; RR 1.68 [95% CI 1.29-2.19], p=0.0003) and ischaemia-driven target lesion revascularisation (5.3% [

126 get vessel-related myocardial infarction, or ischaemia-driven target lesion revascularisation) and th

127 get vessel-related myocardial infarction, or ischaemia-driven target lesion revascularisation).

128 ardiac mortality, all myocardial infarction, ischaemia-driven target lesion revascularisation, and al

129 These include ischaemia due to immune-mediated microvascular injury, e

130 There were no clinical signs of bowel ischaemia during the follow-up period.

131 ent, the restoration of blood flow following ischaemia elicits a profound inflammatory response media

132 t affecting their amplitude, suggesting that ischaemia enhances vesicular glutamate release from pres

133 n mature oligodendrocytes and that, although ischaemia evokes a glutamate-triggered membrane current,

134 In pathology, ischaemia evokes capillary constriction by pericytes.

135 g (RIPC), induced by intermittent periods of ischaemia followed by reperfusion, confers cardiovascula

136 nditioning (RIPC), induced by brief bouts of ischaemia followed by reperfusion, confers vascular adap

137 sing a non-human primate model of myocardial ischaemia followed by reperfusion, we show that cryopres

138 gies to protect cardiomyocytes vulnerable to ischaemia, for example during cardiac ischaemia or surge

139 ic brain regions of a mouse cerebral hypoxia-ischaemia (H/I) model.

140 hether individuals with transient myocardial ischaemia had different autonomic responses to the stres

141 that patients with more severe resting limb ischaemia have a larger BP response to exercise.

142 n a neonatal rat model of unilateral hypoxia-ischaemia (HI), the effect of five different HT temperat

143 ons that protect against subsequent bouts of ischaemia; however, the effect of RIPC repeated over sev

144 ng is a physiological response after hypoxia-ischaemia; however, the potential neuroprotective effect

145 nce tissue regeneration and attenuate tissue ischaemia; however, their contribution to the immune reg

146 o improve neurological outcomes after global ischaemia-hypoxia in comatose patients who have had card

147 rapeutic hypothermia after transient hypoxia-ischaemia in a piglet model of perinatal asphyxia using

148 cinate is a universal metabolic signature of ischaemia in a range of tissues and is responsible for m

149 emains the preferred technique for assessing ischaemia in bedside situations, whereas CT has the grea

150 Femoral artery ligation-induced ischaemia in mice increases CatK expression and activity

151 Transient focal cerebral ischaemia in mice induced entry of astrocytic mitochondr

152 amage was assured in all animals by surgical ischaemia in pigs with human sized livers (1.2-1.6 kg li

153 y to [(11)C]PK11195 in experimental cerebral ischaemia in rats.

154 point to a distinct tissue response to acute ischaemia in the ageing brain and merit validation studi

155 bstantial overlap in symptoms and signs with ischaemia in the anterior circulation.

156 nts with neurological symptoms suggestive of ischaemia in the area of the MCA within 12 hours followi

157 vesicular glutamate release during in vitro ischaemia in the calyx of Held terminal, an experimental

158 and LV remodelling in response to myocardial ischaemia in vivo.

159 cellular and whole-heart models of simulated ischaemia, in keeping with the clinical association of h

160 During early ischaemia, increased Ca(2+) influx into presynaptic term

161 coronary artery perivascular fibrosis, with ischaemia indicated by enhanced cardiomyocyte Hif1a expr

162 rmed to investigate if UDCA protects against ischaemia-induced and reperfusion-induced arrhythmias in

163 dministration reduced the incidence of acute ischaemia-induced arrhythmias (p = 0.028), with a reduct

164 ce stroke, at least in part, by exacerbating ischaemia-induced BBB disruption.

165 Ca(2+) uptake via NCX underlies the ischaemia-induced Ca(2+) rise and the consequent increas

166 tion and Ca(2+) uptake via NCX underlies the ischaemia-induced Ca(2+) rise and the consequent increas

167 extracellular Na(+) completely inhibited the ischaemia-induced Ca(2+) rise.

168 rmeability transition and protecting against ischaemia-induced cardiomyocyte necrosis and heart failu

169 The ischaemia-induced increase in presynaptic Ca(2+) was med

170 KB-R7943, an inhibitor of NCX, prevented the ischaemia-induced increases in presynaptic Ca(2+) and ve

171 and replace ventricular myocardium lost from ischaemia-induced infarct.

172 reveal that cathepsin K (CatK) has a role in ischaemia-induced neovascularization.

173 e the role of C3a-C3a receptor signalling in ischaemia-induced neural plasticity, we subjected C3a re

174 g a TTI for drugs intended for prevention of ischaemia-induced ventricular fibrillation (VF).

175 We found that ischaemia-induced vesicular glutamate release was depend

176 al fluid drainage, white matter rarefaction, ischaemia, inflammation, myelin damage, and secondary ne

177 expression is reactivated in adult ECs after ischaemia insults.

178 tures were detected and found to change upon ischaemia; intensities of downfield resonances were foun

179 ETATION: Among patients with recent cerebral ischaemia, intensive antiplatelet therapy did not reduce

180 An early consequence of brain ischaemia is an increase in vesicular glutamate release

181 ess is augmented as the burden of myocardial ischaemia is increased.

182 This response is augmented as the burden of ischaemia is increased.

183 Early ischaemia is related to poor acute neurological status a

184 ABSTRACT: Chronic muscle ischaemia leads to accumulation of lactic acid and other

185 thological inverse responses occurred during ischaemia (<18 ml/100 g/min) thus exacerbating perfusion

186 Chronic limb ischaemia may sensitize muscle afferents and potentiate

187 HS treatment improved cardiac function after ischaemia (mean +/- SD for area under the curve, AUC, fo

188 icated in cellular responses to seizures and ischaemia, mechanisms for intrinsic plasticity and cell

189 for cortical [lactate] as a marker of tissue ischaemia/metabolism detected lower levels in TLN-treate

190 In a mouse hindlimb ischaemia model, we examine the effects of hMSCs in whic

191 gulants are likely to reduce recurrent brain ischaemia more effectively than are antiplatelet drugs.

192 In ischaemia myelin is damaged in a Ca(2+)-dependent manner

193 ectronic medical records from the Myocardial Ischaemia National Audit Project and the General Practic

194 and Wales were obtained from the Myocardial Ischaemia National Audit Project between January 1, 2003

195 score analyses, of data from the Myocardial Ischaemia National Audit Project for patients presenting

196 and Welsh registry data from the Myocardial Ischaemia National Audit Project.

197 ormobaric oxygen therapy administered during ischaemia nearly completely prevents the neuronal death,

198 ce from rodent studies that even brief focal ischaemia not resulting in tissue infarction can cause e

199 Early ischaemia occurred in 40 (66%) with a mean DWI/ADC volum

200 081) to identify the effect on bleeding and ischaemia of a long (12-24 months) or short (3-6 months)

201 cular events in patients with acute cerebral ischaemia of atherosclerotic origin.

202 When grafted into brains subjected to global ischaemia, Olig2PC-Astros exhibit superior neuroprotecti

203 sh the relative effect of donor age and cold ischaemia on kidneys from circulatory-death and brain-de

204 ed microneurography to assess the effects of ischaemia on single human sympathetic fibres innervating

205 ry cycles (VRCs) could detect the effects of ischaemia on sympathetic nerve fibres.

206 study documents the effect of global cardiac ischaemia on the mechanisms of VF.

207 nosed and occluded arteries leading to organ ischaemia or hypertension, and for aneurysmal disease.

208 reatment-related adverse events: two cardiac ischaemia or infarction, one hypomagnesaemia, and one pa

209 One (<1%) patient had grade 4 cardiac ischaemia or infarction.

210 this barrier can occur during inflammation, ischaemia or sepsis and cause severe organ dysfunction.

211 ble to ischaemia, for example during cardiac ischaemia or surgery.

212 n of Connexin43 phosphorylation during acute ischaemia (p = 0.0027).

213 r 50% its control value as early as 3-h post ischaemia, paralleling the onset of cytotoxic oedema.

214 tion achieved through post-handgrip-exercise ischaemia (PEI) and beta1 -adrenergic receptor (AR) bloc

215 s matched for LV length during post-exercise ischaemia (PEI) and beta1 -adrenergic receptor blockade.

216 uscle metaboreflex activation (post-exercise ischaemia; PEI) following leg cycling exercise, (3) isom

217 Following renal ischaemia, Pgc1alpha(-/-) (also known as Ppargc1a(-/-))

218 iew that age related neuron vulnerability to ischaemia plays a role in stroke and other age related n

219 atment of symptomatic patients or those with ischaemia-producing coronary lesions, and reduces ischae

220 n these findings, we conclude that a reduced ischaemia propensity and attenuated upstream reactive fi

221 We hypothesized that reduced ischaemia propensity in VOH compared to POH accounted fo

222 osis, structural and haemodynamic factors of ischaemia propensity, and the activation of profibrotic

223 tings of pathological cardiac hypertrophy or ischaemia protects the heart against progression to hear

224 Nevertheless, ischaemia raises oligodendrocyte [Ca(2+)]i, [Mg(2+)]i an

225 an mPTP antagonist with clinical efficacy in ischaemia reperfusion injury, equivalently prevent mPTP

226 ion have reduced I(MCU) and are resistant to ischaemia reperfusion injury, myocardial infarction and

227 ion and programmed cell death in response to ischaemia reperfusion injury.

228 is efficacious in an animal model of kidney ischaemia reperfusion injury.

229 Although mitochondrial ROS production in ischaemia reperfusion is established, it has generally b

230 t protein kinase II (CaMKII) is activated in ischaemia reperfusion, myocardial infarction and neurohu

231 ible for mitochondrial ROS production during ischaemia reperfusion.

232 potential (m) depolarization during no-flow ischaemia-reperfusion (I-R) remain controversial, at lea

233 tudy the chicken embryo heart in response to ischaemia-reperfusion (IR) injury.

234 ice, blocks vascular permeability induced by ischaemia-reperfusion (IR), restores depressed cardiac f

235 acking MG53 show increased susceptibility to ischaemia-reperfusion and overventilation-induced injury

236 agents, anti-adhesion agents, modulators of ischaemia-reperfusion and oxidative stress, agents that

237 s a potential therapeutic target to decrease ischaemia-reperfusion injury in a range of pathologies.

238 hibition is sufficient to ameliorate in vivo ischaemia-reperfusion injury in murine models of heart a

239 ficacy of mirococept (APT070) for preventing ischaemia-reperfusion injury in the kidney allograft (EM

240 in vitro and on ferroptosis-associated renal ischaemia-reperfusion injury in vivo.

241 Ischaemia-reperfusion injury occurs when the blood suppl

242 Severe ischaemia-reperfusion injury of the right kidney, with s

243 els of lung, bowel and skin inflammation and ischaemia-reperfusion injury relevant to myocardial infa

244 Because of the potential ischaemia-reperfusion injury to the kidney, we hypothesi

245 2 (Nrf2) affords protection against cerebral ischaemia-reperfusion injury via the upregulation of ant

246 cluding neuromuscular diseases of childhood, ischaemia-reperfusion injury, and age-related neurodegen

247 anistic basis for cell therapy in mice after ischaemia-reperfusion injury, and find that-although hea

248 in atherosclerosis, vascular and myocardial ischaemia-reperfusion injury, and heart failure, and we

249 nsights have emerged regarding mechanisms of ischaemia-reperfusion injury, and some hold promise as t

250 diac excitability and cytoprotection against ischaemia-reperfusion injury, in part, by opening myocar

251 w revisits the pathophysiology of myocardial ischaemia-reperfusion injury, including the role of auto

252 is, diabetic vascular complications, cardiac ischaemia-reperfusion injury, myocardial infarction, hea

253 In the setting of ischaemia-reperfusion injury, RIP1 is deacetylated in a

254 vide significant clinical protection against ischaemia-reperfusion injury, Type II diabetes and agein

255 s and pathophysiological processes including ischaemia-reperfusion injury.

256 d functional rejuvenation to the heart after ischaemia-reperfusion injury.

257 unifies many hitherto unconnected aspects of ischaemia-reperfusion injury.

258 d protection by IMD (1 nmol l(-)(1)) against ischaemia-reperfusion injury.

259 protects hearts from oxidative damage after ischaemia-reperfusion or hypoxia-reoxygenation by mainta

260 In isolated rat hearts subjected to an ischaemia-reperfusion protocol, left ventricular dysfunc

261 e efficacy and safety of nerinetide in human ischaemia-reperfusion that occurs with rapid endovascula

262 cardiomyopathy, atherosclerosis, damage from ischaemia-reperfusion, cardiac hypertrophy and decompens

263 can ameliorate experimental AKI triggered by ischaemia-reperfusion, toxic injury and systemic inflamm

264 non-vascular cells from oxidative stress and ischaemia-reperfusion,predominantly via AM1 receptors.

265 ation is a recognised mediator of myocardial ischaemia-reperfusion-injury (IRI) and cardiomyocytes ar

266 is effective in preclinical stroke models of ischaemia-reperfusion.

267 In the setting of ischaemia/reperfusion (I/R) in the heart, activation of

268 t PI3Kdelta inhibition confers protection in ischaemia/reperfusion models of stroke.

269 tochondrial uncoupling, and protects against ischaemia/reperfusion.

270 atients, and SNRK reduces infarct size after ischaemia/reperfusion.

271 The early events of IFNgamma-induced tumour ischaemia resemble non-apoptotic blood vessel regression

272 AChA territory spared or ischaemia restricted to MT only, compared with other par

273 Myocardial ischaemia resulting from obstructive coronary artery dis

274 lcium and ATP, mitochondrial depolarization, ischaemia-sensitive leak current, and time to K(ir) 6.2

275 Treatments addressing acute ischaemia should be evaluated for their effect on outcom

276 h results from other brain regions, in vitro ischaemia significantly increased the frequency of spont

277 f neurological disorders, including cerebral ischaemia, sleep apnoea, Alzheimer's disease, multiple s

278 Here we show that during ischaemia, soluble CD163 functions as a decoy receptor f

279 nts (death, myocardial infarction, recurrent ischaemia, stroke, and heart failure) at 90 days.

280 In the context of ischaemia, the myocardium is deprived of oxygen and nutr

281 al attacks (TNAs) are due to vertebrobasilar ischaemia, then they should be common during the days an

282 Under conditions of ischaemia, there is a directionally opposite autonomic r

283 However, under conditions of myocardial ischaemia, there was a directionally opposite cardiac au

284 ctors of sICH were: thrombolysis in cerebral ischaemia (TICI) score, Alberta stroke program early CT

285 The warm ischaemia time for the graft after removal was 4 min and

286 time was 9.3 (3.5-18.5) h versus median cold ischaemia time of 8.9 (4.2-11.4) h.

287 e graft after removal was 4 min and the cold ischaemia time was 16 h.

288 stomised cutting guides that aimed to reduce ischaemia time.

289 emia-producing coronary lesions, and reduces ischaemia to a greater extent than medical treatment.

290 val for the first phase 2A clinical trial of ischaemia-tolerant mesenchymal stem cells to treat Alzhe

291 increased glutamate release during in vitro ischaemia, using pre- and postsynaptic whole-cell record

292 cose deprivation (OGD), an in vitro model of ischaemia, via a pathway involving the unfolded protein

293 ailure include paracetamol toxicity, hepatic ischaemia, viral and autoimmune hepatitis, and drug-indu

294 The propensity for ischaemia was more important in POH versus VOH, explaini

295 imaging showed that the penumbra of cerebral ischaemia was narrower in the active-phase mouse model t

296 with CT-visible evidence of recent cerebral ischaemia were at increased risk of thrombotic events.

297 e incidence of VF caused by 120 min regional ischaemia were contrasted with its concurrent adverse ef

298 te carotid artery occlusion and haemodynamic ischaemia, were examined for evidence of stroke related

299 e of blood flow and consequently in cerebral ischaemia, which can cause secondary injury in the peri-

300 ring endovascular treatment of critical limb ischaemia with severe rest pain.