ライフサイエンスコーパス: brain ischemia

1 as a model for studying natural tolerance to brain ischemia.

2 he hippocampus and subventricular zone after brain ischemia.

3 pathology of neurological conditions such as brain ischemia.

4 te in apoptotic and necrotic processes after brain ischemia.

5 oxygen-glucose deprivation (OGD) to simulate brain ischemia.

6 dil reduced brain injury in animal models of brain ischemia.

7 roprotective agent in animal models of focal brain ischemia.

8 hippocampal neurons vulnerable to transient brain ischemia.

9 and DNA methylation in vivo after mild focal brain ischemia.

10 , and thrombosis, any of which may result in brain ischemia.

11 a major determinant of cell injury following brain ischemia.

12 Secondary end point was brain ischemia.

13 x may contribute to neuronal apoptosis after brain ischemia.

14 ning outcome following both global and focal brain ischemia.

15 secondary derangements include posttraumatic brain ischemia.

16 s on the various vascular lesions that cause brain ischemia.

17 lization by brain tissue without evidence of brain ischemia.

18 cids may be one potential ligand of TREM2 in brain ischemia.

19 p at 126 days of gestation after exposure to brain ischemia.

20 l death, inflammation and angiogenesis after brain ischemia.

21 angements and cell edema without evidence of brain ischemia.

22 -targeted approach to rescuing neurons after brain ischemia.

23 ramidal neurons after recurrent seizures and brain ischemia.

24 bstantially to secondary tissue injury after brain ischemia.

25 death of functional neurons after transient brain ischemia.

26 hemodynamic variables and for prevention of brain ischemia.

27 in several animal models of global and focal brain ischemia.

28 onal death in a clinically relevant model of brain ischemia.

29 ntegrity of the neurovascular unit following brain ischemia.

30 reases serum levels of S100B, a biomarker of brain ischemia.

31 opioid agonist as efficacious treatments for brain ischemia.

32 cits were significantly worsened after focal brain ischemia.

33 le cerebral artery occlusion (MCAO) model of brain ischemia.

34 ctor of the rat hippocampus following global brain ischemia.

35 opental is neuroprotective in the setting of brain ischemia.

36 neurological conditions such as epilepsy and brain ischemia.

37 dministrations in a mouse model of transient brain ischemia.

38 onis 1 (CA1) in an animal model of transient brain ischemia.

39 etuses with and without exposure to in utero brain ischemia.

40 nd provide a critical overview of reversible brain ischemia.

41 in the cerebral cortex of fetuses exposed to brain ischemia.

42 ransmission in brain and in the pathology of brain ischemia.

43 diated by this pathway in conditions such as brain ischemia.

44 artery occlusive lesions caused hemodynamic brain ischemia.

45 at 1, 2, 3 and 7 days after transient global brain ischemia (12.5 min) in ventilated normothermic rat

46 s are increased in the cerebral cortex after brain ischemia, a condition that induces ER stress.

47 ion inhibition (TI) is observed in transient brain ischemia, a condition that induces persistent TI e

48 nephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circ

49 During brain ischemia, an excessive release of glutamate trigge

50 were excluded due to extracarotid sources of brain ischemia and 4 were excluded due to carotid occlus

51 cular development and aging and in models of brain ischemia and Alzheimer's disease.

52 PA-mediated brain hemorrhage after transient brain ischemia and embolic stroke in rodents.

53 hondrial dysfunction appears to occur during brain ischemia and following reperfusion.

54 28+/-0.34 respectively), but severity of the brain ischemia and hence ligand uptake in the lesion app

55 In acidic conditions such as generated by brain ischemia and hypoxia, especially in association wi

56 important role in neuronal cell death after brain ischemia and in late-onset neurodegenerative disea

57 s; such enhancers may be useful for treating brain ischemia and other hypoxic conditions.

58 iochemical and morphologic effects of global brain ischemia and reperfusion following cardiac arrest.

59 eter strategies to treat patients with acute brain ischemia and severe stenosis of intracranial large

60 of excitotoxic glutamate in animal models of brain ischemia and stroke; however, clinical trials of g

61 TRIF signaling does not confer protection in brain ischemia and suggests the possibility of additiona

62 acterize early BBB disruption in human focal brain ischemia and tested for associations with reperfus

63 e long-term neurological outcome after focal brain ischemia and that the effects may be mediated by a

64 mproves long-term neurological outcome after brain ischemia and the mechanisms for this neuroprotecti

65 bMed, and Google Scholar on terms including "brain ischemia" and "perfusion imaging." The search was

66 % (95% confidence interval, 11.4%-17.1%) for brain ischemia, and 0.7% (95% confidence interval, 0.4%-

67 role in a mouse model of multiple sclerosis, brain ischemia, and Alexander disease.

68 ariety of pathological conditions, including brain ischemia, and cause an acute disruption of synapti

69 athological syndromes such as heart failure, brain ischemia, and stroke.

70 placement tests at 4 days and 4 weeks after brain ischemia, and that infarct volume was increased in

71 We used animal models for experimental brain ischemia as a paradigm of acute brain lesions and

72 8 to 45 years with PFO and no other cause of brain ischemia, as part of the IPSYS registry (Italian P

73 lumes and behavioral deficits after cortical brain ischemia, attenuated cerebral proinflammatory cyto

74 ug with neuroprotective effects in models of brain ischemia attributable to inhibition of brain sodiu

75 ide important insight into the mechanisms of brain ischemia but also demonstrate the complexity of th

76 Cerebral injury may occur not only during brain ischemia but also during reperfusion afterward.

77 peripheral artery disease, had an episode of brain ischemia caused by severe preocclusive carotid art

78 Global brain ischemia causes cell death in the CA1 region of th

79 Brain ischemia causes oxygen and glucose deprivation (OG

80 We have previously shown that brain ischemia causes rapid dephosphorylation of Kv2.1 s

81 Convincing evidence has shown that brain ischemia causes the proliferation of neural stem c

82 Thus, brain ischemia compromises NK cell-mediated immune defen

83 intracranial large arteries in patients with brain ischemia depend on the extent of infarction, the l

84 sted that rats subjected to transient global brain ischemia develop depressed expression of GluR-B in

85 In brain ischemia, gating of postsynaptic glutamate recepto

86 itrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W

87 optotic and necrotic mechanisms may occur in brain ischemia, immunohistochemical changes of BNIP3 wer

88 Diabetes influences brain ischemia in a number of different ways.

89 ed CpG oligodeoxynucleotide before transient brain ischemia in mice confers substantial protection ag

90 protective effects following transient focal brain ischemia in rats.

91 ees C) after traumatic brain injury or focal brain ischemia in various species.

92 gulated by macrophages/microglia after focal brain ischemia in vivo.

93 [K(+)] ([K(+)](E)) is highly elevated during brain ischemia, in vitro studies aimed at explaining the

94 ension has given way to a focus on secondary brain ischemia, in which cerebral perfusion pressure and

95 Nuclear location of BNIP3 after brain ischemia indicates a novel role for the regulation

96 Here we have determined whether brain ischemia-induced amplification of the NSCs/NPCs in

97 The role of brain ischemia-induced NSC/NPC proliferation, however, h

98 Acute brain ischemia induces a local neuroinflammatory reactio

99 Brain ischemia induces an inflammatory response involvin

100 Focal brain ischemia induces inflammation, extracellular matri

101 Brain ischemia induces the toxic accumulation of unfolde

102 tly reduced hippocampal neuronal death after brain ischemia, inhibited the ischemia-induced inflammat

103 Brain ischemia inhibits immune function systemically, wi

104 Reversible brain ischemia is a harbinger for subsequent ischemic st

105 released from membrane phospholipids during brain ischemia is a major source of lipid peroxides.

106 rventional treatment of acute and threatened brain ischemia is a rapidly changing field.

107 e most important predictor of risk following brain ischemia is degree of early clinical reversibility

108 Brain ischemia is responsible for significant morbidity

109 The function of MANF during brain ischemia is still not known.

110 nary resuscitation model and other models of brain ischemia is that the effects of asphyxic cardiac a

111 est that the upregulation of OPN after focal brain ischemia may play a role in cellular (glia, macrop

112 nvestigated the mechanistic link among acute brain ischemia, microbiota alterations, and the immune r

113 bral ischemia and reperfusion injury in this brain ischemia model.

114 Brain ischemia occurs when the blood supply to the brain

115 ffects of DHA in pathological models such as brain ischemia or Alzheimer's disease.

116 ss observed in the striatum following global brain ischemia or in Huntington's disease.

117 In addition, brain ischemia (postmortem exposure) was not associated

118 In global brain ischemia, protective-preservative mild hypothermia

119 of r-Hu-EPO before or up to 6 h after focal brain ischemia reduced injury by approximately 50-75%.

120 ing (2% isoflurane for 30 min at 24 h before brain ischemia) reduced brain infarct sizes and improved

121 cclusion (tMCAO) model was used to establish brain ischemia-reperfusion injury.

122 tive stress contributes to neuronal death in brain ischemia-reperfusion.

123 the SIRT3 role in mitochondrial response to brain ischemia/reperfusion (IR) showed that SIRT3-mediat

124 xamined the role of Tregs after experimental brain ischemia/reperfusion injury.

125 ngly, a robust p53-CypD complex forms during brain ischemia/reperfusion injury.

126 er than anti-leukocyte recruitment following brain ischemia/reperfusion injury.

127 In the brain, ischemia/reperfusion (IR) triggered rearrangement

128 Brain ischemia results from cardiac arrest, stroke or he

129 iac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.

130 ced neurodegeneration by two models of focal brain ischemia/stroke and by glutamate receptor-mediated

131 To establish whether NOX2 plays a role in brain ischemia, strokes were created in mice, then mice

132 A brief period of global brain ischemia, such as that induced by cardiac arrest o

133 cellular pathways that link SMC function to brain ischemia susceptibility.

134 lutamate receptors, a condition occurring in brain ischemia that down-regulates GABAB receptors, cons

135 that vascular amyloid contributes to chronic brain ischemia, therefore amyloid burden measured by Pit

136 During early stages of brain ischemia, transient SMC but not pericyte constrict

137 oxic conditions, which are characteristic of brain ischemia, traumatic brain injury, and neurodegener

138 y is emerging as an important component of a brain ischemia treatment program.

139 trophic factors are neuroprotective and that brain ischemia-triggered NSC/NPC proliferation is crucia

140 LOTBUST trial (Combined Lysis of Thrombus in Brain Ischemia Using Transcranial Ultrasound and Systemi

141 Cortical brain ischemia was produced in 16-18 month-old transgeni

142 ell proliferation, for the first 7days after brain ischemia was used to block ischemia-induced NSC/NP

143 impaired written naming of verbs after focal brain ischemia, we combined imaging and behavioral testi

144 In vivo, in rats subjected to thromboembolic brain ischemia, we found that intraischemic helium at 75

145 ink the formation of SGs to TI and DND after brain ischemia, we investigated SG induction in brain re

146 Using a mouse model of transient focal brain ischemia, we report that IL-21 is highly up-regula

147 The rates of the secondary end point brain ischemia were also similar in the 2 treatment grou

148 This contrasts with previous findings in brain ischemia, where Doav and T2 appear to be uncorrela

149 After traumatic brain injury or focal brain ischemia, which seem to still benefit from even la

150 nt approaches to improve outcome after focal brain ischemia will likely be derived by looking at natu

151 d whether minocycline protects against focal brain ischemia with a wide therapeutic window.