ライフサイエンスコーパス: focal cerebral ischemia

1 neurodegenerative diseases and stroke (i.e., focal cerebral ischemia).

2 os and hsp70 mRNA were examined during acute focal cerebral ischemia.

3 he amount of DNA fragmentation at 24 h after focal cerebral ischemia.

4 are neuroprotective when administered after focal cerebral ischemia.

5 sible involvement in the brain's response to focal cerebral ischemia.

6 ombo-inflammatory brain infarction following focal cerebral ischemia.

7 hase (NOS) either ameliorates or exacerbates focal cerebral ischemia.

8 then subjected to transient left hemisphere focal cerebral ischemia.

9 ations of EBA immunohistochemistry following focal cerebral ischemia.

10 effect on infarction volume following severe focal cerebral ischemia.

11 the risk of hemorrhagic transformation after focal cerebral ischemia.

12 al blood flow (rCBF) changes during moderate focal cerebral ischemia.

13 ses of clomethiazole in models of global and focal cerebral ischemia.

14 sampling of 2-mg brain tissue in a model of focal cerebral ischemia.

15 F, and NADH redox state during 3 h of severe focal cerebral ischemia.

16 critical step in apoptotic cell death after focal cerebral ischemia.

17 via upregulation of neurotrophins, following focal cerebral ischemia.

18 t to the MCA of anesthetized rats to produce focal cerebral ischemia.

19 fore or 60 mins after the onset of permanent focal cerebral ischemia.

20 -mediated tissue damage and BBB breakdown in focal cerebral ischemia.

21 europathological outcome in animal models of focal cerebral ischemia.

22 bumin therapy is markedly neuroprotective in focal cerebral ischemia.

23 ar proteolysis, and neuronal degeneration in focal cerebral ischemia.

24 uced by iNOS influences COX-2 activity after focal cerebral ischemia.

25 al contusion and to reduce brain edema after focal cerebral ischemia.

26 reduces neurological damage after transient focal cerebral ischemia.

27 ear in a subpopulation of microvessels after focal cerebral ischemia.

28 mice are partially protected from transient, focal cerebral ischemia.

29 ts of fingolimod in several rodent models of focal cerebral ischemia.

30 sis and associated neuromigration induced by focal cerebral ischemia.

31 arct volume and attenuates brain edema after focal cerebral ischemia.

32 cerebral infarction in mice after transient focal cerebral ischemia.

33 roinflammation, and functional outcome after focal cerebral ischemia.

34 ar filament is a widely used model to induce focal cerebral ischemia.

35 and cognitive tasks up to 3 weeks following focal cerebral ischemia.

36 HIF-1alpha that were subjected to transient focal cerebral ischemia.

37 ich may facilitate functional recovery after focal cerebral ischemia.

38 administered T3 to mice undergoing transient focal cerebral ischemia.

39 on and a dramatically worsened outcome after focal cerebral ischemia.

40 mplement proteins (C1q, C3, C5) to transient focal cerebral ischemia.

41 dy neuronal degeneration following temporary focal cerebral ischemia.

42 IA, PtdCho-PLC, and CCTalpha after transient focal cerebral ischemia.

43 ex (ASR) was sensitive to lesions induced by focal cerebral ischemia.

44 al outcome in both head trauma and transient focal cerebral ischemia.

45 eptide, has an 8-h therapeutic window in rat focal cerebral ischemia.

46 usion from 1 to 3 hours in rats subjected to focal cerebral ischemia.

47 , on CSD-induced tolerance against transient focal cerebral ischemia.

48 d in the hemisphere ipsilateral to transient focal cerebral ischemia.

49 hemic striatum and cerebral cortex following focal cerebral ischemia.

50 mation in an experimental model of transient focal cerebral ischemia.

51 NA expression and ADC reduction during acute focal cerebral ischemia.

52 knockouts compared with wild-type mice after focal cerebral ischemia.

53 rogrammed cell death (PCD) in many models of focal cerebral ischemia.

54 infarct volumes by 40-53% in a rat model of focal cerebral ischemia.

55 s cell death pathway after a brief period of focal cerebral ischemia.

56 arginine increases brain injury in models of focal cerebral ischemia.

57 reduction in infarct volume after transient focal cerebral ischemia.

58 Focal cerebral ischemia (45 min) was induced in anesthet

59 dose of free CDP-choline (by 26%) after 1 h focal cerebral ischemia and 24 h reperfusion in spontane

60 Damage to neurons caused by focal cerebral ischemia and epileptic seizures was exace

61 hat enhance neuron survival during transient focal cerebral ischemia and excitotoxin-induced seizures

62 havioral and histopathological outcome after focal cerebral ischemia and head trauma.

63 (E2) on BBB disruption induced by transient focal cerebral ischemia and its effects on MMP2 and MMP9

64 en free radical generation during reversible focal cerebral ischemia and its relationship to nitric o

65 that the MEK/ERK pathway is activated during focal cerebral ischemia and may play a role in inducing

66 s as an endogenous neuroprotective factor in focal cerebral ischemia and may therefore represent a ta

67 Experimental stroke using a focal cerebral ischemia and reperfusion (FCIR) model was

68 their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) for the pr

69 their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) tissue inj

70 mice (MT-TG) affords protection against mild focal cerebral ischemia and reperfusion.

71 ncreased expression of MT-1 protects against focal cerebral ischemia and reperfusion.

72 ments were performed using a murine model of focal cerebral ischemia and reperfusion.

73 tion and apoptotic neuronal cell death after focal cerebral ischemia and reperfusion.

74 ssing hsp72 improves neuron survival against focal cerebral ischemia and systemic kainic acid adminis

75 K pathway contributes to brain injury during focal cerebral ischemia and that PD98059, a MEK1-specifi

76 immune response decreases infarct size after focal cerebral ischemia and that sensitization to the sa

77 Focal cerebral ischemia and traumatic brain injury induc

78 s STAT3 activation in female rat brain after focal cerebral ischemia and whether STAT3 activation con

79 In murine models of focal cerebral ischemia, APC provided remarkable anti-in

80 diffusion coefficient of water (ADC) during focal cerebral ischemia are often reversible with reperf

81 Animal models of focal cerebral ischemia are well accepted for investigat

82 ondary to anaerobic metabolism during severe focal cerebral ischemia attenuates NOS activity.

83 t be activated by multiple mechanisms during focal cerebral ischemia, Bid is critical to its early ac

84 oncluded that estrogen rescues neurons after focal cerebral ischemia by increasing the level of Bcl-2

85 r wt littermates were subjected to permanent focal cerebral ischemia by intraluminal blockade of the

86 ry VEGF isoform VEGF165b in a mouse model of focal cerebral ischemia by middle cerebral artery occlus

87 We produced focal cerebral ischemia by middle cerebral artery occlus

88 sly hypertensive rats subjected to 60 min of focal cerebral ischemia by permanent ligation of the rig

89 e pathophysiology of Alzheimer's disease and focal cerebral ischemia, cerebrovascular M(5) receptors

90 peri-infarct area at 3 days after permanent focal cerebral ischemia compared to the sham-operated no

91 ntioxidant that, in a rat model of transient focal cerebral ischemia, confers significant enduring fu

92 stroke, we used a murine model of transient focal cerebral ischemia consisting of intraluminal middl

93 Focal cerebral ischemia elicits an inflammatory response

94 cytochrome c in vivo occurs after permanent focal cerebral ischemia (FCI) and is mediated by the mit

95 on of gelatinases before and after transient focal cerebral ischemia (FCI) in mice.

96 ytochrome c in vivo occurred after transient focal cerebral ischemia (FCI) in rats and preceded the p

97 Focal cerebral ischemia (FCI) induces rapid neuronal dea

98 ERK1/2 and oxidative stress after transient focal cerebral ischemia (FCI) using transgenic (Tg) mice

99 ion occur following neural injury, including focal cerebral ischemia (fci).

100 Male C57BL/6 mice were subjected to 1h of focal cerebral ischemia followed by 24 or 72 h of reperf

101 ormed before, during, and after induction of focal cerebral ischemia from 1 h to 7 days.

102 etrimental roles for the gelatinase MMP-9 in focal cerebral ischemia, how dysregulated MMP proteolysi

103 Transient focal cerebral ischemia in adult mice was induced by lig

104 in areas of developing neovasculature after focal cerebral ischemia in adult rat.

105 file of nestin expression after induction of focal cerebral ischemia in adult rats.

106 ount of hemisphere enlargement after 24 h of focal cerebral ischemia in both knockout mutants of SOD1

107 intraluminal suture method for induction of focal cerebral ischemia in genetically altered mice incl

108 e brain, we analyzed the effect of transient focal cerebral ischemia in ICAM-1-deficient mice generat

109 effects of gender and estrogen treatment on focal cerebral ischemia in male and female rats.

110 d this possibility in the model of transient focal cerebral ischemia in mice bearing a disruption of

111 WF reduces infarct volume up to 2-fold after focal cerebral ischemia in mice, thus showing the import

112 g the 2 week recovery period after transient focal cerebral ischemia in mice.

113 ases 1 and 2 (ERK 1/2) were activated during focal cerebral ischemia in mice.

114 es neurological deficits following permanent focal cerebral ischemia in rats.

115 22 prevents ischemic damage to the BBB after focal cerebral ischemia in rats.

116 ticipate in delayed cortical responses after focal cerebral ischemia in rats.

117 administered FGF-13 in a model of permanent focal cerebral ischemia in Sprague-Dawley rats.

118 on of protein kinase C (PKC) after transient focal cerebral ischemia in SV-129 mice were assessed by

119 eceptors, was measured after transient (1 h) focal cerebral ischemia in the mouse middle cerebral art

120 d to validate a modified method of temporary focal cerebral ischemia in the mouse; neurobehavioral fu

121 omoter elements were investigated after mild focal cerebral ischemia in the rat.

122 is saturated (P50) on outcome from transient focal cerebral ischemia in the rat.

123 ective when administered after initiation of focal cerebral ischemia in the rat.

124 lectin mediated leukocyte infiltration after focal cerebral ischemia in the rat.

125 roprotective potential of PROG in a model of focal cerebral ischemia in the rat.

126 Here, we show that after focal cerebral ischemia in vivo or oxygen-glucose depriv

127 nd that NMDA exposure in vitro and transient focal cerebral ischemia in vivo resulted in increased le

128 s increased by neuronal hypoxia in vitro and focal cerebral ischemia in vivo, and that neuronal survi

129 a and reduced infarct volume after permanent focal cerebral ischemia induced by middle cerebral arter

130 HS to rats (at a nonsedating dose) following focal cerebral ischemia induced by middle cerebral arter

131 Here we found that focal cerebral ischemia induced by middle cerebral/commo

132 size and improves functional outcome, after focal cerebral ischemia induced by occlusion of the midd

133 We showed that focal cerebral ischemia induced nestin lineage neural st

134 Focal cerebral ischemia induces morphological changes (e

135 After permanent focal cerebral ischemia induction, infarct volume and ne

136 Focal cerebral ischemia initiates self-repair mechanisms

137 Focal cerebral ischemia is associated with expression of

138 um ion homeostasis during re-perfusion after focal cerebral ischemia is caused by cellular rather tha

139 e interaction between nitric oxide (NO.) and focal cerebral ischemia is multifaceted.

140 However, the effect of ERK 1/2 activation in focal cerebral ischemia is still unclear.

141 lammatory mediator, whose source and role in focal cerebral ischemia is worth studying.

142 Focal cerebral ischemia, known as stroke, causes serious

143 c period following a 2-h period of transient focal cerebral ischemia leads to a reduction of cortical

144 Transient focal cerebral ischemia leads to extensive neuronal dama

145 rly in vivo, adult NR3A TG mice subjected to focal cerebral ischemia manifested less damage than WT m

146 After 90 min of transient focal cerebral ischemia, MMP-9 null mice receiving wild-

147 on induces neuronal apoptosis in a transient focal cerebral ischemia model in mice.

148 perfusion injury to brain tissue caused by a focal cerebral ischemia model in rats.

149 portant in cell survival pathways, we used a focal cerebral ischemia model to examined whether SHP2 i

150 Bid, in ischemic neuronal death in a murine focal cerebral ischemia model.

151 pharmacological inhibition of PARP in a rat focal cerebral ischemia model.

152 l ischemia reperfusion damage in a transient focal cerebral ischemia model.

153 This data suggests that during severe focal cerebral ischemia, NO. mechanisms of injury have a

154 Specific knockdown of MMP-12 after focal cerebral ischemia offers neuroprotection that coul

155 influence of preserving hypertension during focal cerebral ischemia on stroke outcome in a rat model

156 her treatment with HBO initiated early after focal cerebral ischemia-onset protects the brain when ex

157 ain trauma, localized brain edema, hematoma, focal cerebral ischemia, or brain tumors.

158 In focal cerebral ischemia, peri-infarct depolarizations (P

159 In a mouse model of focal cerebral ischemia, reactive astrocytes in the peri

160 In mice, transient focal cerebral ischemia reduced endogenous ARC protein i

161 Tat-N-dimer (3 nmol/g) to mice subjected to focal cerebral ischemia reduces infarct volume with 40%

162 report that the extent of brain injury after focal cerebral ischemia reperfusion is increased, and be

163 ic borderzone vascular density 10 days after focal cerebral ischemia-reperfusion in rats.

164 (SOD-NPs) and tested their efficacy in a rat focal cerebral ischemia-reperfusion injury model.

165 ctional component in neuroregeneration after focal cerebral ischemia-reperfusion.

166 euronal death and reduce infarct volume in a focal cerebral ischemia/reperfusion mouse model.

167 ity and subsequent apoptosis associated with focal cerebral ischemia/reperfusion.

168 This model of embolic focal cerebral ischemia results in ischemic cell damage

169 (18)[F]-fluorodeoxyglucose immediately after focal cerebral ischemia showed increased glucose uptake

170 ChRs), as long as 6 hours after the onset of focal cerebral ischemia significantly reduces brain inju

171 rs in JNK-mediated apoptosis after transient focal cerebral ischemia (tFCI), which, when induced by 6

172 m of O(2)(*-) overproduction after transient focal cerebral ischemia (tFCI).

173 2, are significantly reduced after transient focal cerebral ischemia (tFCI).

174 ly decreased in mouse brains after transient focal cerebral ischemia (tFCI).

175 reduces apoptotic cell death after transient focal cerebral ischemia (tFCI).

176 used for identifying the ischemic lesion in focal cerebral ischemia, the understanding of spatiotemp

177 cise means of quantitating BBB disruption in focal cerebral ischemia; this method will be of consider

178 tes can be seen chronologically in permanent focal cerebral ischemia using 1H magnetic resonance spec

179 thetic estrogens were examined in a model of focal cerebral ischemia using 210 male, intact female, a

180 te and time of administration in relation to focal cerebral ischemia, VEGF can improve histological o

181 Reversible or permanent focal cerebral ischemia was created by intraluminal midd

182 er the neuroprotective efficacy of MK-801 in focal cerebral ischemia was dependent on strain and/or v

183 tor knock-out mice, mortality from permanent focal cerebral ischemia was increased, infarct size and

184 Transient focal cerebral ischemia was induced by a 90 min period o

185 Focal cerebral ischemia was induced by a transient (90 m

186 Focal cerebral ischemia was induced by embolic middle ce

187 Focal cerebral ischemia was induced by intraluminal fila

188 Focal cerebral ischemia was induced by permanent distal

189 Focal cerebral ischemia was induced by permanently clipp

190 Focal cerebral ischemia was induced by transient (1h) oc

191 Two hours after the end of EA pretreatment, focal cerebral ischemia was induced following 24h reperf

192 Focal cerebral ischemia was induced in Long-Evans rats b

193 Focal cerebral ischemia was induced in mice (by permanen

194 In Long-Evans rats, focal cerebral ischemia was produced by cauterization of

195 Focal cerebral ischemia was produced by occlusion of the

196 Transient focal cerebral ischemia was produced for 2 hrs with the

197 Temporary focal cerebral ischemia was produced in rats by middle c

198 ivity following CNS injury, a mouse model of focal cerebral ischemia was utilized to study SHP-1 expr

199 function of TNF from this cellular source in focal cerebral ischemia we used TNF conditional knock ou

200 role of reperfusion in DNA damage following focal cerebral ischemia, we determined the distribution

201 igate its dose dependent effect on permanent focal cerebral ischemia, we examined neurological defici

202 In a model of experimental focal cerebral ischemia, we have recently reported a str

203 ze and neurological deficits after transient focal cerebral ischemia were more severe, cerebral blood

204 protein nitration, and neuronal death after focal cerebral ischemia were significantly reduced in tr

205 ng pathway for apoptosis following permanent focal cerebral ischemia where there is no reperfusion in

206 ed on observations in vivo that treatment of focal cerebral ischemia with EPO enhances the migration

207 tested this hypothesis in an animal model of focal cerebral ischemia without reperfusion.