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1 nfarct volume in rats subjected to transient focal ischemia.
2 tro and in vivo brain slice-based models for focal ischemia.
3 uced on the rat cortex 1 day after transient focal ischemia.
4 cerebral infarction 24 hours after permanent focal ischemia.
5 ine receptor on brain damage after transient focal ischemia.
6 brain injury in rats subjected to permanent focal ischemia.
7 injury after a prolonged period 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 n of human PRP attenuates brain injury after focal ischemia.
15 pment of neuronal injury following transient focal ischemia.
16 microvascular perfusion induced by permanent focal ischemia.
17 uroprotective effects of 619C89 in temporary focal ischemia.
18 holipases in neuronal injury after transient focal ischemia.
19 bral infarction in a rat model of reversible focal ischemia.
20 europrotective in a mouse model of transient focal ischemia.
21 e properties, in a rodent model of transient focal ischemia.
22 erebral infarction occurring after transient focal ischemia.
23 for targeted therapeutic interventions after focal ischemia.
24 cells in the SVZ and dentate gyrus following focal ischemia.
25 ributes to neurovascular injury during acute focal ischemia.
26 microglia in the brains of rats subjected to focal ischemia.
27 lso decreased infarct size in a rat model of focal ischemia.
28 le cerebral artery occlusion (MCAO) model of focal ischemia.
29 ffective after ipsilateral and contralateral focal ischemia.
30 onclusion, RIP attenuates brain injury after focal ischemia.
31 ction in endogenously born neurons following focal ischemia.
32 ere investigated in a rat model of temporary focal ischemia.
33 otected neurons from death in vivo following focal ischemia.
34 issue that is damaged but not yet dead after focal ischemia.
35 significantly reduced infarct volumes after focal ischemia.
36 cerebral artery occlusion model of transient focal ischemia.
37 into the damaged region in aged brain after focal ischemia.
38 ent was found in aged rats given FGF-2 after focal ischemia.
39 and down-regulated in ischemic tissues after focal ischemia.
40 eurological recovery in rodents subjected to focal ischemia.
41 thermic conditions in this neonatal model of focal ischemia.
42 the volume of damage in a model of neonatal focal ischemia.
43 xic edema and necrotic neuronal death during focal ischemia.
44 manner, as determined at 3 d after 90 min of focal ischemia.
45 d wild-type mice were subjected to transient focal ischemia.
46 ined the effects of APC in a murine model of focal ischemia.
47 contribute to lesion expansion during acute focal ischemia.
48 ice (-67% and -41%, respectively) after mild focal ischemia.
49 ects of the injury cascade that occurs after focal ischemia.
54 orate brain injury in experimental adult rat focal ischemia and in a mild neonatal hypoxia-ischemia (
55 expression profiles of rat brains following focal ischemia and performed computational analysis of c
56 c mice overexpressing SOD2 undergo transient focal ischemia and reperfusion followed by assessment of
58 ght is now shifting towards emphasizing both focal ischemia and subsequent reperfusion in developing
59 PARP activation in neuronal damage following focal ischemia and suggest that therapies designed towar
61 rom the effects of glutamate excitotoxicity, focal ischemia, and 1-methyl-4-phenyl-1,2,3,6-tetrahydro
62 has been observed in adult rats subjected to focal ischemia, and expression of these transcription fa
63 ression (SD) has been demonstrated following focal ischemia, and the additional workload imposed by S
64 ide one explanation for the vascular injury, focal ischemia, and thrombosis observed in acute vascula
65 es in survival signaling following temporary focal ischemia, and thus may represent an attractive tar
67 aspects of this popular method for transient focal ischemia as it applies to the mouse are discussed.
68 e is thus neuroprotective in both global and focal ischemia at plasma concentrations known to be well
69 -Kyoto rats [WKY]) when exposed to transient focal ischemia; b) infarction size is not correlated wit
71 against cerebral injury following transient focal ischemia but that prolonged hypothermia is require
72 n the first 4 h is highly neuroprotective in focal ischemia, but it is unknown whether delayed albumi
73 ed as mediators of neuronal damage following focal ischemia, but their molecular targets have not bee
74 S isoform contributes to tissue damage after focal ischemia by amplifying excitotoxic amino acid rele
76 hip between these pathways in a rat model of focal ischemia by observing and modifying the activation
77 In rabbit hearts subjected to global and focal ischemia, CcO activity was inhibited in a time-dep
78 ignificantly increased infarct volumes after focal ischemia compared with WT littermate controls.
80 Postnatal day 7 rat pups were subjected to focal ischemia followed by global hypoxia and then admin
81 very from ischemic injury and that temporary focal ischemia for even 8-minute duration can cause dela
86 PA neither aggravated brain damage caused by focal ischemia in a filament model of middle carotid art
88 that was significantly down-regulated after focal ischemia in adult rats as well as after oxygen-glu
94 can significantly reduce brain damage after focal ischemia in rats and displays a low toxicity in vi
102 er, there have been no controlled studies of focal ischemia in the rat under alpha-chloralose anesthe
105 that has been shown to be neuroprotective in focal ischemia in vivo and is currently in phase I/II cl
106 survival and becomes nuclear in response to focal ischemia in vivo and when cultured neurons are dep
108 smaller infarcts when subjected to transient focal ischemia, indicating a detrimental role of S129 ph
109 d cerebral blood flow by 26% following acute focal ischemia induced by middle cerebral artery occlusi
113 ses to motor rehabilitative training in vivo Focal ischemia instigated a period of synapse turnover i
115 nfarct volume in a rodent model of transient focal ischemia involving either 2 or 6h of ischemia.
116 e nitric oxide synthase (NOS)-2 in permanent focal ischemia is not clear, we examined its expression
117 w of therapeutic opportunity after transient focal ischemia is rather brief and that critical mechani
118 ial hyperthermia superimposed upon transient focal ischemia markedly enhances calpain activation and
120 ects of MMP-9 gene knock-out after transient focal ischemia may be mediated by reduced proteolytic de
121 al expression of transcription factors after focal ischemia may reflect the potential for neuronal re
122 dependent neuroprotective effects in a brain focal ischemia model and direct cellular effects on huma
128 cortical neurons and in vivo mouse cerebral focal ischemia models of preconditioning, cellular injur
129 ed that LncRNA FosDT induced after transient focal ischemia modulates poststroke behavioral deficits
131 ops during recirculation, we studied whether focal ischemia of the same duration, followed by reperfu
132 e for 7 days were subjected to 60 minutes of focal ischemia on post-discontinuation day 0 (D-0) or D-
133 d with premiR-29c and subjected to transient focal ischemia, post-ischemic miR-29c levels were restor
137 (NO(2)(-)) increases cellular resilience to focal ischemia/reperfusion injury in multiple organs.
140 r pathways, we employ a VaD mouse model with focal ischemia replicating many elements of the complex
145 nly pretreatment has previously been used in focal ischemia, the objective of the present study was t
146 physiological recordings in a mouse model of focal ischemia to demonstrate that PIDs are associated w
148 fluctuations of calcium ions associated with focal ischemia using a molecular functional MRI approach
149 eased COX-2 activity in a model of transient focal ischemia using a transgenic mouse model in which h
157 nal variation in metabolites after permanent focal ischemia were investigated longitudinally in rats
158 that HBO can improve outcome after temporary focal ischemia when treatment is started early after isc
159 (MCAo) model in the rat, an animal model of focal ischemia, when given both prior to and after the o
160 tral neurons from excitotoxicity, as well as focal ischemia, whereas axons in the nucleus, probably c
161 area is restricted 1 day after the transient focal ischemia, while CBF responses are intact in normal
162 in ischemic tissue at prolonged times after focal ischemia, while reductions in tissue amounts of gl
163 olume, and brain swelling in a rat transient focal ischemia with hyperglycemia model, suggesting that