ライフサイエンスコーパス: focal ischemia

1 uced on the rat cortex 1 day after transient focal ischemia.

2 cerebral infarction 24 hours after permanent focal ischemia.

3 ine receptor on brain damage after transient focal ischemia.

4 n of human PRP attenuates brain injury after focal ischemia.

5 brain injury in rats subjected to permanent focal ischemia.

6 injury after a prolonged period of transient focal ischemia.

7 europrotective in a mouse model of transient focal ischemia.

8 rat brain at 6, 24, and 48 h after permanent focal ischemia.

9 erted into the ischemic periphery after 24 h focal ischemia.

10 ng the over-expression of APP mRNA following focal ischemia.

11 d with wild-type littermates after permanent focal ischemia.

12 brain injury in a feline model of transient focal ischemia.

13 agmentation following permanent or transient focal ischemia.

14 pment of neuronal injury following transient focal ischemia.

15 microvascular perfusion induced by permanent focal ischemia.

16 uroprotective effects of 619C89 in temporary focal ischemia.

17 holipases in neuronal injury after transient focal ischemia.

18 bral infarction in a rat model of reversible focal ischemia.

19 e properties, in a rodent model of transient focal ischemia.

20 erebral infarction occurring after transient focal ischemia.

21 cells in the SVZ and dentate gyrus following focal ischemia.

22 ributes to neurovascular injury during acute focal ischemia.

23 microglia in the brains of rats subjected to focal ischemia.

24 lso decreased infarct size in a rat model of focal ischemia.

25 le cerebral artery occlusion (MCAO) model of focal ischemia.

26 ffective after ipsilateral and contralateral focal ischemia.

27 onclusion, RIP attenuates brain injury after focal ischemia.

28 ction in endogenously born neurons following focal ischemia.

29 ere investigated in a rat model of temporary focal ischemia.

30 eurological recovery in rodents subjected to focal ischemia.

31 otected neurons from death in vivo following focal ischemia.

32 issue that is damaged but not yet dead after focal ischemia.

33 significantly reduced infarct volumes after focal ischemia.

34 cerebral artery occlusion model of transient focal ischemia.

35 into the damaged region in aged brain after focal ischemia.

36 ent was found in aged rats given FGF-2 after focal ischemia.

37 and down-regulated in ischemic tissues after focal ischemia.

38 thermic conditions in this neonatal model of focal ischemia.

39 the volume of damage in a model of neonatal focal ischemia.

40 xic edema and necrotic neuronal death during focal ischemia.

41 tro and in vivo brain slice-based models for focal ischemia.

42 manner, as determined at 3 d after 90 min of focal ischemia.

43 d wild-type mice were subjected to transient focal ischemia.

44 ined the effects of APC in a murine model of focal ischemia.

45 contribute to lesion expansion during acute focal ischemia.

46 ice (-67% and -41%, respectively) after mild focal ischemia.

47 ects of the injury cascade that occurs after focal ischemia.

48 nfarct volume in rats subjected to transient focal ischemia.

49 he ventrolateral medulla following transient focal ischemia affect cardiovascular functions.

50 Focal ischemia also increased FosDT binding to chromatin

51 Transient focal ischemia also significantly upregulated serine-129

52 Rats that were subjected to 90 min focal ischemia and 7 d recovery were given MnTE-2-PyP(5+

53 orate brain injury in experimental adult rat focal ischemia and in a mild neonatal hypoxia-ischemia (

54 expression profiles of rat brains following focal ischemia and performed computational analysis of c

55 c mice overexpressing SOD2 undergo transient focal ischemia and reperfusion followed by assessment of

56 o induce neuroprotection in animal models of focal ischemia and spinal cord injury.

57 PARP activation in neuronal damage following focal ischemia and suggest that therapies designed towar

58 unctional outcome improves in rats following focal ischemia and treatment with 3-AB.

59 rom the effects of glutamate excitotoxicity, focal ischemia, and 1-methyl-4-phenyl-1,2,3,6-tetrahydro

60 has been observed in adult rats subjected to focal ischemia, and expression of these transcription fa

61 ression (SD) has been demonstrated following focal ischemia, and the additional workload imposed by S

62 ide one explanation for the vascular injury, focal ischemia, and thrombosis observed in acute vascula

63 es in survival signaling following temporary focal ischemia, and thus may represent an attractive tar

64 Rats underwent 90 minutes of focal ischemia, and tPA infusion was begun 10 minutes pr

65 aspects of this popular method for transient focal ischemia as it applies to the mouse are discussed.

66 e is thus neuroprotective in both global and focal ischemia at plasma concentrations known to be well

67 -Kyoto rats [WKY]) when exposed to transient focal ischemia; b) infarction size is not correlated wit

68 After 2 h of focal ischemia, both groups of rats showed similar degre

69 against cerebral injury following transient focal ischemia but that prolonged hypothermia is require

70 n the first 4 h is highly neuroprotective in focal ischemia, but it is unknown whether delayed albumi

71 ed as mediators of neuronal damage following focal ischemia, but their molecular targets have not bee

72 S isoform contributes to tissue damage after focal ischemia by amplifying excitotoxic amino acid rele

73 After permanent focal ischemia by middle cerebral artery occlusion, the

74 hip between these pathways in a rat model of focal ischemia by observing and modifying the activation

75 In rabbit hearts subjected to global and focal ischemia, CcO activity was inhibited in a time-dep

76 ignificantly increased infarct volumes after focal ischemia compared with WT littermate controls.

77 Postnatal day 7 rat pups were subjected to focal ischemia followed by global hypoxia and then admin

78 very from ischemic injury and that temporary focal ischemia for even 8-minute duration can cause dela

79 Following focal ischemia, GLT-1 mRNA expression was decreased sign

80 The murine model of focal ischemia, however, remains incompletely characteri

81 We induced focal ischemia in 12 rats using the middle cerebral arte

82 ined in a neonatal model employing transient focal ischemia in a 7-day-old rat pup.

83 PA neither aggravated brain damage caused by focal ischemia in a filament model of middle carotid art

84 tly reduced infarct size following permanent focal ischemia in a mouse model of ischemic stroke.

85 that was significantly down-regulated after focal ischemia in adult rats as well as after oxygen-glu

86 Six hours of focal ischemia in cats (n = 10) was produced by permanen

87 of NKCC1 protein was increased following 2-h focal ischemia in cerebral cortex.

88 yloid precursor protein (APP) mRNA following focal ischemia in female rats.

89 ema formation and infarction after permanent focal ischemia in mice.

90 of MCP-1 protein expression after permanent focal ischemia in mice.

91 can significantly reduce brain damage after focal ischemia in rats and displays a low toxicity in vi

92 a mediator of brain injury during permanent focal ischemia in rats.

93 mia (30 degrees C) on these activities after focal ischemia in rats.

94 of the brain from damage produced by distal focal ischemia in rats.

95 ic border regions after 90 mins of transient focal ischemia in the cat.

96 Focal ischemia in the cerebral cortex results in acute a

97 Thus, focal ischemia in the P7 rat produces different distribu

98 We tested whether RIP protects against focal ischemia in the rat brain.

99 er, there have been no controlled studies of focal ischemia in the rat under alpha-chloralose anesthe

100 ibute to cerebral infarction after transient focal ischemia in the rat.

101 in the dorsal horn of the dentate gyrus and focal ischemia in the striatum.

102 that has been shown to be neuroprotective in focal ischemia in vivo and is currently in phase I/II cl

103 survival and becomes nuclear in response to focal ischemia in vivo and when cultured neurons are dep

104 preading depression (SD) on the evolution of focal ischemia in vivo.

105 smaller infarcts when subjected to transient focal ischemia, indicating a detrimental role of S129 ph

106 d cerebral blood flow by 26% following acute focal ischemia induced by middle cerebral artery occlusi

107 ic alcohol consumption exacerbates transient focal ischemia-induced brain damage.

108 of chronic alcohol consumption on transient focal ischemia-induced brain damage.

109 In focal ischemia, intracerebroventricular injection of ASI

110 nfarct volume in a rodent model of transient focal ischemia involving either 2 or 6h of ischemia.

111 e nitric oxide synthase (NOS)-2 in permanent focal ischemia is not clear, we examined its expression

112 w of therapeutic opportunity after transient focal ischemia is rather brief and that critical mechani

113 ial hyperthermia superimposed upon transient focal ischemia markedly enhances calpain activation and

114 MK2(-/-) mice subjected to focal ischemia markedly reduced infarct size by 64 and 7

115 ects of MMP-9 gene knock-out after transient focal ischemia may be mediated by reduced proteolytic de

116 al expression of transcription factors after focal ischemia may reflect the potential for neuronal re

117 dependent neuroprotective effects in a brain focal ischemia model and direct cellular effects on huma

118 A transient focal ischemia model with C57Bl/6 mice was used to inves

119 In a rat focal ischemia model, caspase-3 enzymatic activity, as r

120 he neuroprotective effect of PC in the mouse focal ischemia model.

121 monstrate the efficacy of NRG-1 in pMCAO rat focal ischemia model.

122 recovery from neurological deficits in a rat focal ischemia model.

123 cortical neurons and in vivo mouse cerebral focal ischemia models of preconditioning, cellular injur

124 ed that LncRNA FosDT induced after transient focal ischemia modulates poststroke behavioral deficits

125 Transient focal ischemia of brief duration (15-30 min) gives rise

126 ops during recirculation, we studied whether focal ischemia of the same duration, followed by reperfu

127 e for 7 days were subjected to 60 minutes of focal ischemia on post-discontinuation day 0 (D-0) or D-

128 d with premiR-29c and subjected to transient focal ischemia, post-ischemic miR-29c levels were restor

129 itro findings, a survival model of rat heart focal ischemia-reperfusion (I-R) was investigated.

130 tive protective effects in a rodent model of focal ischemia-reperfusion.

131 uroprotective effects were examined in mouse focal ischemia/reperfusion (I/R) model.

132 (NO(2)(-)) increases cellular resilience to focal ischemia/reperfusion injury in multiple organs.

133 mage and a defective functional outcome in a focal ischemia/reperfusion model of stroke.

134 s a therapeutic agent in the murine model of focal ischemia/reperfusion.

135 Thus, experimental focal ischemia simulating TIAs can: induce Hsp70 protein

136 This study examined very brief focal ischemia that simulates transient ischemic attacks

137 After focal ischemia, the degree of infarction decreases with

138 In a mouse model of transient focal ischemia, the inhibitor reduced infarct sizes both

139 nly pretreatment has previously been used in focal ischemia, the objective of the present study was t

140 physiological recordings in a mouse model of focal ischemia to demonstrate that PIDs are associated w

141 We currently report that transient focal ischemia upregulates alpha-Syn protein expression

142 eased COX-2 activity in a model of transient focal ischemia using a transgenic mouse model in which h

143 Focal ischemia was created by inserting a 3-0 surgical s

144 Focal ischemia was induced by a 2-h occlusion of the mid

145 Transient focal ischemia was induced by occluding both common caro

146 Transient focal ischemia was induced by occluding the left middle

147 Focal ischemia was induced by temporary occlusion of the

148 Transient focal ischemia was induced in control (wild type) and MT

149 More importantly, using a rat model of focal ischemia, we demonstrated that systemic applicatio

150 nal variation in metabolites after permanent focal ischemia were investigated longitudinally in rats

151 that HBO can improve outcome after temporary focal ischemia when treatment is started early after isc

152 (MCAo) model in the rat, an animal model of focal ischemia, when given both prior to and after the o

153 tral neurons from excitotoxicity, as well as focal ischemia, whereas axons in the nucleus, probably c

154 area is restricted 1 day after the transient focal ischemia, while CBF responses are intact in normal

155 in ischemic tissue at prolonged times after focal ischemia, while reductions in tissue amounts of gl

156 olume, and brain swelling in a rat transient focal ischemia with hyperglycemia model, suggesting that

157 in injury and HT in a rat model of transient focal ischemia with hyperglycemia.

158 and/or L contribute to cerebral injury after focal ischemia with reperfusion.