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1 onist MK801-in mouse and rat models of focal cerebral ischaemia.
2 brain of naive rats and animals subjected to cerebral ischaemia.
3 ned to yield rapid flow restoration in acute cerebral ischaemia.
4 ts therapeutic potential in a mouse model of cerebral ischaemia.
5 on outcome in the first 24 h after transient cerebral ischaemia.
6 lammation and neuronal damage in response to cerebral ischaemia.
7 ameliorated blood-brain barrier damage after cerebral ischaemia.
8 endogenous repair mechanisms activated after cerebral ischaemia.
9 l cascade that produces cell death following cerebral ischaemia.
10 ting recurrent events in patients with acute cerebral ischaemia.
11 time course of GADD34 expression after focal cerebral ischaemia.
12 ssessing neuronal damage in rodent models of cerebral ischaemia.
13  progressive neuronal injury observed during cerebral ischaemia.
14 der to restore depleted energy stores during cerebral ischaemia.
15 er resistance to normally lethal episodes of cerebral ischaemia.
16 rovide more robust neuroprotection in global cerebral ischaemia.
17  a small degree of neuroprotection in global cerebral ischaemia.
18 NMDA) receptor in the gerbil model of global cerebral ischaemia.
19 cal cascade that occurs during and following cerebral ischaemia.
20  sensitivity to experimentally induced focal cerebral ischaemia.
21 haemia-induced brain damage following global cerebral ischaemia.
22 uced neuronal damage in rat models of global cerebral ischaemia.
23 logy of neuronal death after transient focal cerebral ischaemia.
24 n's disease, known single gene disorders and cerebral ischaemia.
25 ts of LY231617 in the gerbil model of global cerebral ischaemia.
26 oagulants for atrial fibrillation (AF) after cerebral ischaemia.
27 ith high rates of rebleeding, vasospasm, and cerebral ischaemia.
28 acerebral haemorrhage, and early and delayed cerebral ischaemia.
29 mpair this mechanism, increasing the risk of cerebral ischaemia.
30 ticoagulants), and 1447 patients with AF and cerebral ischaemia.
31 nclear whether CPP augmentation could reduce cerebral ischaemia, a finding which might prompt the sea
32                                    Following cerebral ischaemia, a significant benefit of progesteron
33 tomy in patients with evidence of reversible cerebral ischaemia across the 6-24 h time window and are
34 y constitute a new cell therapy for treating cerebral ischaemia and other neurological diseases.
35 nnel blockers strongly reduce EAA release in cerebral ischaemia and other pathological states associa
36                                        Focal cerebral ischaemia and post-ischaemic reperfusion cause
37  -5 and TIMP-3 expression after experimental cerebral ischaemia and to examine whether cytokines know
38 ng depression increased sensitivity to focal cerebral ischaemia, and blocking of cortical spreading d
39 xicities: palmar-plantar erythrodysesthesia, cerebral ischaemia, and deep-vein thrombosis.
40 sses cell type-specific mechanisms of global cerebral ischaemia, and examines the circumstances in wh
41 ly related to the extent of damage following cerebral ischaemia, and the targeting of this inflammati
42                                              Cerebral ischaemia appears to be an important mechanism
43                       Rodent models of focal cerebral ischaemia are critical for understanding pathop
44 ents with intracranial artery dissection and cerebral ischaemia are treated with antithrombotics.
45 strated evidence of ipsilateral haemodynamic cerebral ischaemia as measured by PET OEF, while 50 (64.
46  in the first 24 h following transient focal cerebral ischaemia by using mice with each isoform genet
47                                       In the cerebral ischaemia cohort (779 with SVD), during 3366 pa
48  controlled model of brain injury induced by cerebral ischaemia combined with fast in vivo two-photon
49 en regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal s
50 ored for clinical/radiological cVSP, delayed cerebral ischaemia (DCI), and 3-month functional outcome
51 y stenosis but no recent stroke or transient cerebral ischaemia, either carotid artery stenting (CAS)
52 ial growth factor-A (VEGF-A), upregulated in cerebral ischaemia; endothelin-1 (EDN1), a mediator of v
53 nd sheds new light on the pathophysiology of cerebral ischaemia following brain injury.
54 ynthase (nNOS) inhibitor, in three models of cerebral ischaemia (global gerbil, global rat and focal
55                                        Early cerebral ischaemia has been characterized further, with
56 nd gene products upon the pathophysiology of cerebral ischaemia has been greatly enhanced by the use
57          The neocortical clip model of focal cerebral ischaemia has previously been used with success
58 ulnerability to stroke and outcome following cerebral ischaemia have frequently been observed and att
59 the cellular and biochemical consequences of cerebral ischaemia in acute ischaemic stroke (AIS) have
60 cts of progesterone administration following cerebral ischaemia in aged and ovariectomized mice.
61                              Transient focal cerebral ischaemia in mice induced entry of astrocytic m
62                     A simple model of global cerebral ischaemia in mouse is bilateral common carotid
63 d directly to [(11)C]PK11195 in experimental cerebral ischaemia in rats.
64 glycaemia in vitro and both global and focal cerebral ischaemia in vivo.
65 del of global and in two rat models of focal cerebral ischaemia in vivo.
66   INTERPRETATION: Among patients with recent cerebral ischaemia, intensive antiplatelet therapy did n
67 uroprotective efficacy of enadoline in focal cerebral ischaemia is due to inhibition of glutamate rel
68 evated extracellular glycine during or after cerebral ischaemia may induce excessive NMDA/glutamate r
69              This increases the risk of IH), cerebral ischaemia, neuroinflammation and lacunar infarc
70 cardiovascular events in patients with acute cerebral ischaemia of atherosclerotic origin.
71 A1 cell loss by transient 4-vessel occlusion cerebral ischaemia on the subsequent development of the
72                   No studies using models of cerebral ischaemia or TBI assessed efficacy when progest
73 ective role of progesterone following either cerebral ischaemia or TBI importantly it highlights area
74  in a dose-dependent manner following either cerebral ischaemia (P < 0.001) or TBI (P = 0.03) with th
75 inistered immediately following (i.e. 0-2 h) cerebral ischaemia (P = 0.0008).
76 complications such as hydrocephalus, delayed cerebral ischaemia related to microvascular dysfunction
77 d factor 2 (Nrf2) affords protection against cerebral ischaemia-reperfusion injury via the upregulati
78 a on mitochondrial function damage following cerebral ischaemia/reperfusion, Mongolian gerbils were s
79            Future neuroprotection studies in cerebral ischaemia require stringent monitoring of cereb
80 a range of neurological disorders, including cerebral ischaemia, sleep apnoea, Alzheimer's disease, m
81 e, hypertension, coronary-bypass surgery and cerebral ischaemia, smoking and body mass index for indi
82       During neurodegenerative disorders and cerebral ischaemia, the accumulation of immature and den
83 ictive factors of sICH were: thrombolysis in cerebral ischaemia (TICI) score, Alberta stroke program
84                      In patients with AF and cerebral ischaemia treated with anticoagulants, we compa
85                                        Focal cerebral ischaemia was induced by transient middle cereb
86 -speckle imaging showed that the penumbra of cerebral ischaemia was narrower in the active-phase mous
87  patients with CT-visible evidence of recent cerebral ischaemia were at increased risk of thrombotic
88 -induced hippocampal damage in gerbil global cerebral ischaemia when dosed at 10, 12.5 (P<0.05) or 15
89 a decrease of blood flow and consequently in cerebral ischaemia, which can cause secondary injury in