ライフサイエンスコーパス: cerebral ischaemia

1 ameliorated blood-brain barrier damage after cerebral ischaemia.

2 ting recurrent events in patients with acute cerebral ischaemia.

3 brain of naive rats and animals subjected to cerebral ischaemia.

4 ned to yield rapid flow restoration in acute cerebral ischaemia.

5 ts therapeutic potential in a mouse model of cerebral ischaemia.

6 on outcome in the first 24 h after transient cerebral ischaemia.

7 lammation and neuronal damage in response to cerebral ischaemia.

8 endogenous repair mechanisms activated after cerebral ischaemia.

9 l cascade that produces cell death following cerebral ischaemia.

10 der to restore depleted energy stores during 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 er resistance to normally lethal episodes of cerebral ischaemia.

15 rovide more robust neuroprotection in global cerebral ischaemia.

16 a small degree of neuroprotection in global cerebral ischaemia.

17 NMDA) receptor in the gerbil model of global cerebral ischaemia.

18 cal cascade that occurs during and following cerebral ischaemia.

19 sensitivity to experimentally induced focal cerebral ischaemia.

20 haemia-induced brain damage following global cerebral ischaemia.

21 uced neuronal damage in rat models of global cerebral ischaemia.

22 logy of neuronal death after transient focal cerebral ischaemia.

23 n's disease, known single gene disorders and cerebral ischaemia.

24 ts of LY231617 in the gerbil model of global cerebral ischaemia.

25 nclear whether CPP augmentation could reduce cerebral ischaemia, a finding which might prompt the sea

26 Following cerebral ischaemia, a significant benefit of progesteron

27 y constitute a new cell therapy for treating cerebral ischaemia and other neurological diseases.

28 nnel blockers strongly reduce EAA release in cerebral ischaemia and other pathological states associa

29 Focal cerebral ischaemia and post-ischaemic reperfusion cause

30 -5 and TIMP-3 expression after experimental cerebral ischaemia and to examine whether cytokines know

31 ng depression increased sensitivity to focal cerebral ischaemia, and blocking of cortical spreading d

32 xicities: palmar-plantar erythrodysesthesia, cerebral ischaemia, and deep-vein thrombosis.

33 ly related to the extent of damage following cerebral ischaemia, and the targeting of this inflammati

34 Cerebral ischaemia appears to be an important mechanism

35 Rodent models of focal cerebral ischaemia are critical for understanding pathop

36 ents with intracranial artery dissection and cerebral ischaemia are treated with antithrombotics.

37 strated evidence of ipsilateral haemodynamic cerebral ischaemia as measured by PET OEF, while 50 (64.

38 in the first 24 h following transient focal cerebral ischaemia by using mice with each isoform genet

39 controlled model of brain injury induced by cerebral ischaemia combined with fast in vivo two-photon

40 en regarded as an important cause of delayed cerebral ischaemia (DCI) which occurs after aneurysmal s

41 ored for clinical/radiological cVSP, delayed cerebral ischaemia (DCI), and 3-month functional outcome

42 nd sheds new light on the pathophysiology of cerebral ischaemia following brain injury.

43 ynthase (nNOS) inhibitor, in three models of cerebral ischaemia (global gerbil, global rat and focal

44 Early cerebral ischaemia has been characterized further, with

45 nd gene products upon the pathophysiology of cerebral ischaemia has been greatly enhanced by the use

46 The neocortical clip model of focal cerebral ischaemia has previously been used with success

47 ulnerability to stroke and outcome following cerebral ischaemia have frequently been observed and att

48 cts of progesterone administration following cerebral ischaemia in aged and ovariectomized mice.

49 Transient focal cerebral ischaemia in mice induced entry of astrocytic m

50 A simple model of global cerebral ischaemia in mouse is bilateral common carotid

51 d directly to [(11)C]PK11195 in experimental cerebral ischaemia in rats.

52 glycaemia in vitro and both global and focal cerebral ischaemia in vivo.

53 del of global and in two rat models of focal cerebral ischaemia in vivo.

54 INTERPRETATION: Among patients with recent cerebral ischaemia, intensive antiplatelet therapy did n

55 uroprotective efficacy of enadoline in focal cerebral ischaemia is due to inhibition of glutamate rel

56 evated extracellular glycine during or after cerebral ischaemia may induce excessive NMDA/glutamate r

57 cardiovascular events in patients with acute cerebral ischaemia of atherosclerotic origin.

58 A1 cell loss by transient 4-vessel occlusion cerebral ischaemia on the subsequent development of the

59 No studies using models of cerebral ischaemia or TBI assessed efficacy when progest

60 ective role of progesterone following either cerebral ischaemia or TBI importantly it highlights area

61 in a dose-dependent manner following either cerebral ischaemia (P < 0.001) or TBI (P = 0.03) with th

62 inistered immediately following (i.e. 0-2 h) cerebral ischaemia (P = 0.0008).

63 d factor 2 (Nrf2) affords protection against cerebral ischaemia-reperfusion injury via the upregulati

64 a on mitochondrial function damage following cerebral ischaemia/reperfusion, Mongolian gerbils were s

65 Future neuroprotection studies in cerebral ischaemia require stringent monitoring of cereb

66 a range of neurological disorders, including cerebral ischaemia, sleep apnoea, Alzheimer's disease, m

67 e, hypertension, coronary-bypass surgery and cerebral ischaemia, smoking and body mass index for indi

68 During neurodegenerative disorders and cerebral ischaemia, the accumulation of immature and den

69 Focal cerebral ischaemia was induced by transient middle cereb

70 patients with CT-visible evidence of recent cerebral ischaemia were at increased risk of thrombotic

71 -induced hippocampal damage in gerbil global cerebral ischaemia when dosed at 10, 12.5 (P<0.05) or 15

72 a decrease of blood flow and consequently in cerebral ischaemia, which can cause secondary injury in