ライフサイエンスコーパス: ischaemia

1 naptic terminals in the early phase of brain ischaemia.

2 rce about their ability to reduce angina and ischaemia.

3 Rs are dependent on ASIC1a activation during ischaemia.

4 ation in the ischaemic territory 1 day after ischaemia.

5 ss in the presence and absence of myocardial ischaemia.

6 res at presynaptic terminals during in vitro ischaemia.

7 is defective, resulting in functional muscle ischaemia.

8 flammation and subsequent brain damage after ischaemia.

9 cardiography to detect or exclude myocardial ischaemia.

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

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

12 aired functional recovery following hindlimb ischaemia.

13 ed blood-brain barrier damage after cerebral ischaemia.

14 is protective in a mouse model of myocardial ischaemia.

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

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

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

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

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

20 schaemia and during 20 min of recovery after ischaemia.

21 ity and brain infarction in mice after focal ischaemia.

22 naive rats and animals subjected to cerebral ischaemia.

23 rt and vasculature from oxidative stress and ischaemia.

24 rrent events in patients with acute cerebral ischaemia.

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

26 eld rapid flow restoration in acute cerebral ischaemia.

27 eutic potential in a mouse model of cerebral ischaemia.

28 0 (19 [1%] vs 21 [1%]) had grade 3-5 cardiac ischaemia.

29 l time-lapse fluorescence imaging of cardiac ischaemia.

30 e in the first 24 h after transient cerebral ischaemia.

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

32 significant functional impairment following ischaemia.

33 and neuronal damage in response to cerebral ischaemia.

34 lutamate, which may affect the outcome after ischaemia.

35 s repair mechanisms activated after cerebral ischaemia.

36 that produces cell death following cerebral ischaemia.

37 tion or death in patients with critical limb ischaemia.

38 nt responses to exogenous ET-1 as well as to ischaemia.

39 to play a crucial role in epilepsy and brain ischaemia.

40 store depleted energy stores during cerebral ischaemia.

41 AMPAR subunit composition in the response to ischaemia.

42 the central nervous system during myocardial ischaemia.

43 ould be a therapeutic target in white matter ischaemia.

44 TRPA1 block reduces myelin damage in ischaemia.

45 yte viability under starvation and simulated ischaemia.

46 ccumulation with better renal function after ischaemia.

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

48 ccur only in pathological conditions such as ischaemia.

49 y render the kidney especially vulnerable to ischaemia.

50 naptic terminals in the early phase of brain ischaemia.

51 ive cardiac surgery were subjected to 90 min ischaemia/120 min reoxygenation at 37 degrees C.

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

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

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

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

56 After cardiac ischaemia, a prolonged decrease of coronary microvascula

57 Myocardial ischaemia activates cardiac sympathetic afferents leadin

58 ontractility (miR-21, miR-133a), and hypoxia/ischaemia adaptation (miR-21, miR-146a, and miR-210) wer

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

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

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

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

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

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

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

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 re inhibited before ischaemia or during both ischaemia and reoxygenation.

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

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

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

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

77 lls are early responders to acute intestinal ischaemia and their activation initiates rapid signallin

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

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

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

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

82 CEP promoted angiogenesis in hindlimb ischaemia and wound healing models through MyD88-depende

83 mplications (digital ulceration and critical ischaemia) and discusses possible further developments i

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

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

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

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

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

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

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

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

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

93 es; (ii) administer progesterone solely post-ischaemia; and (iii) combine histopathological and funct

94 pathological features of microvasculitis and ischaemia; and (iv) recognizing the role of inflammation

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

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

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

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

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

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

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

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

103 several early cellular cascades triggered by ischaemia: Ca(2+) influx, Ca(2+) release from intracellu

104 Transient, non-catastrophic brain ischaemia can induce either a protected state against su

105 ve indicated that focal, mild, and transient ischaemia can trigger cortical spreading depression with

106 Ischaemia caused a reproducible, intense and biphasic af

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

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

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

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

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

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

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

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

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

118 Incidence of ischaemia-driven revascularisation and ischaemia-driven

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

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

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

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

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

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

125 paclitaxel-eluting stent had lower rates of ischaemia-driven target lesion revascularisation (9.4%vs

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 3 years, with no significant differences in ischaemia-driven target vessel revascularisation, stent

130 he dose-limiting toxic effect was myocardial ischaemia due to excessive prolongation of systolic ejec

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

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

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

134 Cardiac ischaemia emerged at high plasma concentrations (two pat

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

136 oxin, omega-conotoxin GVIA, each reduced the ischaemia-evoked motor inhibition but not the concurrent

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

138 In pathology, ischaemia evokes capillary constriction by pericytes.

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

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

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

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

143 Patients with critical limb ischaemia have a high rate of amputation and mortality.

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

145 ity to stroke and outcome following cerebral ischaemia have frequently been observed and attributed t

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

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

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

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

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

151 ogesterone administration following cerebral ischaemia in aged and ovariectomized mice.

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

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

154 inhibitors could become a new treatment for ischaemia in patients with angina pectoris.

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

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

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

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

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

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

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

162 have shown that a brief period of myocardial ischaemia increases endothelin in cardiac venous plasma

163 Ischaemia-induced afferent firing was also abrogated by

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

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

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

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

168 looxygenase products contribute primarily to ischaemia-induced changes in intestinal motility.

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 We found that ischaemia-induced vesicular glutamate release was depend

175 expression is reactivated in adult ECs after ischaemia insults.

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

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

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

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

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

181 Early ischaemia is related to poor acute neurological status a

182 otected state against subsequent episodes of ischaemia (ischaemic preconditioning) or delayed, select

183 ng early detection and manipulation of brain ischaemia leading to more individualized treatment.

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

185 loaded with the Ca(2+)-sensitive dye Fura-2, ischaemia leads to an early increase in [Ca(2+)](c) that

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

187 Chronic limb ischaemia may sensitize muscle afferents and potentiate

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 , which occurs when glutamate is released in ischaemia, might cause the anoxic depolarization by evok

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

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

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

194 of ET-1 (n = 7) and to recurrent myocardial ischaemia (n = 7).

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

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

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

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

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

200 After a few minutes of anoxia or ischaemia, neurons in brain slices show a rapid depolari

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

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

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

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

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

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

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

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

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

210 een when PKB and PI-3K were inhibited before ischaemia or during both ischaemia and reoxygenation.

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

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

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

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

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

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

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

218 ts (muscle metaboreflex) using post-exercise ischaemia (PEI) following handgrip partially maintains e

219 oth protocols were followed by post-exercise ischaemia (PEI) to isolate the muscle metaboreflex.

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

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

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

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

224 At 48 h post-ischaemia, progesterone significantly reduced the lesion

225 Whereas in ovariectomized mice, at 48 h post-ischaemia, progesterone treatment had no effect on the a

226 zed mice, allowed to survive for 7 days post-ischaemia, progesterone treatment significantly improved

227 In fact, by 7 days post-ischaemia, progesterone-treated ovariectomized mice did

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

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

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

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

232 dditionally, this study indicates that focal ischaemia provides an experimental paradigm in which to

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

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

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

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

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

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

239 ible for mitochondrial ROS production during ischaemia reperfusion.

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

241 Two episodes of ischaemia-reperfusion (I-R) separated by a 30 min interv

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

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

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

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

246 Ischaemia-reperfusion injury occurs when the blood suppl

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

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

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

250 2 (Nrf2) affords protection against cerebral ischaemia-reperfusion injury via the upregulation of ant

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

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

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

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

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

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

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

258 s and pathophysiological processes including 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 cardiomyopathy, atherosclerosis, damage from ischaemia-reperfusion, cardiac hypertrophy and decompens

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

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

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

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

266 tochondrial uncoupling, and protects against ischaemia/reperfusion.

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

268 Future neuroprotection studies in cerebral ischaemia require stringent monitoring of cerebral blood

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

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

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

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

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

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

275 Five minutes of myocardial ischaemia stimulated all 38 cardiac afferents (8 Adelta,

276 Acute intestinal ischaemia stimulates visceral afferent nerves but the me

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

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

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

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

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

282 dothelin stimulates cardiac afferents during ischaemia through direct activation of endothelin A rece

283 ation of cardiac afferents during myocardial ischaemia through direct stimulation of ET(A) receptors

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

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

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

287 stomised cutting guides that aimed to reduce ischaemia time.

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

289 erone was administered at 1, 6 and 24 h post-ischaemia to aged and ovariectomized female mice.

290 he intestinal tone shortly from the onset of ischaemia to the early period of reperfusion.

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

292 45/TAMARIS), 525 patients with critical limb ischaemia unsuitable for revascularisation were enrolled

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

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

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

296 Acute focal ischaemia was produced by clamping theme senteric vessel

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

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

299 mesenteric afferents during acute intestinal ischaemia, whereas enteric reflex mechanisms and cycloox

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