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1 neurodegenerative diseases and stroke (i.e., focal cerebral ischemia).
2 apoptosis and autophagy following transient focal cerebral ischemia.
3 s cell death pathway after a brief period of focal cerebral ischemia.
4 arginine increases brain injury in models of focal cerebral ischemia.
5 reduction in infarct volume after transient focal cerebral ischemia.
6 on and a dramatically worsened outcome after focal cerebral ischemia.
7 os and hsp70 mRNA were examined during acute focal cerebral ischemia.
8 he amount of DNA fragmentation at 24 h after focal cerebral ischemia.
9 are neuroprotective when administered after focal cerebral ischemia.
10 sible involvement in the brain's response to focal cerebral ischemia.
11 mation in an experimental model of transient focal cerebral ischemia.
12 hase (NOS) either ameliorates or exacerbates focal cerebral ischemia.
13 then subjected to transient left hemisphere focal cerebral ischemia.
14 ations of EBA immunohistochemistry following focal cerebral ischemia.
15 effect on infarction volume following severe focal cerebral ischemia.
16 the risk of hemorrhagic transformation after focal cerebral ischemia.
17 al blood flow (rCBF) changes during moderate focal cerebral ischemia.
18 ses of clomethiazole in models of global and focal cerebral ischemia.
19 sampling of 2-mg brain tissue in a model of focal cerebral ischemia.
20 F, and NADH redox state during 3 h of severe focal cerebral ischemia.
21 critical step in apoptotic cell death after focal cerebral ischemia.
22 via upregulation of neurotrophins, following focal cerebral ischemia.
23 t to the MCA of anesthetized rats to produce focal cerebral ischemia.
24 fore or 60 mins after the onset of permanent focal cerebral ischemia.
25 ombo-inflammatory brain infarction following focal cerebral ischemia.
26 europathological outcome in animal models of focal cerebral ischemia.
27 bumin therapy is markedly neuroprotective in focal cerebral ischemia.
28 ar proteolysis, and neuronal degeneration in focal cerebral ischemia.
29 uced by iNOS influences COX-2 activity after focal cerebral ischemia.
30 al contusion and to reduce brain edema after focal cerebral ischemia.
31 reduces neurological damage after transient focal cerebral ischemia.
32 ear in a subpopulation of microvessels after focal cerebral ischemia.
33 -mediated tissue damage and BBB breakdown in focal cerebral ischemia.
34 mice significantly reduces infarction after focal cerebral ischemia.
35 mice are partially protected from transient, focal cerebral ischemia.
36 ts of fingolimod in several rodent models of focal cerebral ischemia.
37 sis and associated neuromigration induced by focal cerebral ischemia.
38 arct volume and attenuates brain edema after focal cerebral ischemia.
39 cerebral infarction in mice after transient focal cerebral ischemia.
40 roinflammation, and functional outcome after focal cerebral ischemia.
41 and cognitive tasks up to 3 weeks following focal cerebral ischemia.
42 HIF-1alpha that were subjected to transient focal cerebral ischemia.
43 ich may facilitate functional recovery after focal cerebral ischemia.
44 administered T3 to mice undergoing transient focal cerebral ischemia.
45 mplement proteins (C1q, C3, C5) to transient focal cerebral ischemia.
46 dy neuronal degeneration following temporary focal cerebral ischemia.
47 IA, PtdCho-PLC, and CCTalpha after transient focal cerebral ischemia.
48 ex (ASR) was sensitive to lesions induced by focal cerebral ischemia.
49 al outcome in both head trauma and transient focal cerebral ischemia.
50 eptide, has an 8-h therapeutic window in rat focal cerebral ischemia.
51 usion from 1 to 3 hours in rats subjected to focal cerebral ischemia.
52 , on CSD-induced tolerance against transient focal cerebral ischemia.
53 d in the hemisphere ipsilateral to transient focal cerebral ischemia.
54 hemic striatum and cerebral cortex following focal cerebral ischemia.
55 NA expression and ADC reduction during acute focal cerebral ischemia.
56 ar filament is a widely used model to induce focal cerebral ischemia.
57 knockouts compared with wild-type mice after focal cerebral ischemia.
58 rogrammed cell death (PCD) in many models of focal cerebral ischemia.
59 infarct volumes by 40-53% in a rat model of focal cerebral ischemia.
61 dose of free CDP-choline (by 26%) after 1 h focal cerebral ischemia and 24 h reperfusion in spontane
63 hat enhance neuron survival during transient focal cerebral ischemia and excitotoxin-induced seizures
65 (E2) on BBB disruption induced by transient focal cerebral ischemia and its effects on MMP2 and MMP9
66 en free radical generation during reversible focal cerebral ischemia and its relationship to nitric o
67 that the MEK/ERK pathway is activated during focal cerebral ischemia and may play a role in inducing
68 s as an endogenous neuroprotective factor in focal cerebral ischemia and may therefore represent a ta
70 their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) for the pr
71 their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) tissue inj
76 ssing hsp72 improves neuron survival against focal cerebral ischemia and systemic kainic acid adminis
77 K pathway contributes to brain injury during focal cerebral ischemia and that PD98059, a MEK1-specifi
78 immune response decreases infarct size after focal cerebral ischemia and that sensitization to the sa
80 s STAT3 activation in female rat brain after focal cerebral ischemia and whether STAT3 activation con
82 diffusion coefficient of water (ADC) during focal cerebral ischemia are often reversible with reperf
86 t be activated by multiple mechanisms during focal cerebral ischemia, Bid is critical to its early ac
87 oncluded that estrogen rescues neurons after focal cerebral ischemia by increasing the level of Bcl-2
88 r wt littermates were subjected to permanent focal cerebral ischemia by intraluminal blockade of the
90 ry VEGF isoform VEGF165b in a mouse model of focal cerebral ischemia by middle cerebral artery occlus
91 sly hypertensive rats subjected to 60 min of focal cerebral ischemia by permanent ligation of the rig
92 e pathophysiology of Alzheimer's disease and focal cerebral ischemia, cerebrovascular M(5) receptors
93 peri-infarct area at 3 days after permanent focal cerebral ischemia compared to the sham-operated no
94 ntioxidant that, in a rat model of transient focal cerebral ischemia, confers significant enduring fu
95 stroke, we used a murine model of transient focal cerebral ischemia consisting of intraluminal middl
97 cytochrome c in vivo occurs after permanent focal cerebral ischemia (FCI) and is mediated by the mit
99 ytochrome c in vivo occurred after transient focal cerebral ischemia (FCI) in rats and preceded the p
101 ERK1/2 and oxidative stress after transient focal cerebral ischemia (FCI) using transgenic (Tg) mice
103 Male C57BL/6 mice were subjected to 1h of focal cerebral ischemia followed by 24 or 72 h of reperf
105 etrimental roles for the gelatinase MMP-9 in focal cerebral ischemia, how dysregulated MMP proteolysi
109 ount of hemisphere enlargement after 24 h of focal cerebral ischemia in both knockout mutants of SOD1
110 intraluminal suture method for induction of focal cerebral ischemia in genetically altered mice incl
111 e brain, we analyzed the effect of transient focal cerebral ischemia in ICAM-1-deficient mice generat
114 d this possibility in the model of transient focal cerebral ischemia in mice bearing a disruption of
115 WF reduces infarct volume up to 2-fold after focal cerebral ischemia in mice, thus showing the import
122 on of protein kinase C (PKC) after transient focal cerebral ischemia in SV-129 mice were assessed by
123 eceptors, was measured after transient (1 h) focal cerebral ischemia in the mouse middle cerebral art
124 d to validate a modified method of temporary focal cerebral ischemia in the mouse; neurobehavioral fu
131 nd that NMDA exposure in vitro and transient focal cerebral ischemia in vivo resulted in increased le
132 s increased by neuronal hypoxia in vitro and focal cerebral ischemia in vivo, and that neuronal survi
134 a and reduced infarct volume after permanent focal cerebral ischemia induced by middle cerebral arter
135 HS to rats (at a nonsedating dose) following focal cerebral ischemia induced by middle cerebral arter
137 size and improves functional outcome, after focal cerebral ischemia induced by occlusion of the midd
143 um ion homeostasis during re-perfusion after focal cerebral ischemia is caused by cellular rather tha
148 c period following a 2-h period of transient focal cerebral ischemia leads to a reduction of cortical
151 rly in vivo, adult NR3A TG mice subjected to focal cerebral ischemia manifested less damage than WT m
155 portant in cell survival pathways, we used a focal cerebral ischemia model to examined whether SHP2 i
161 influence of preserving hypertension during focal cerebral ischemia on stroke outcome in a rat model
162 her treatment with HBO initiated early after focal cerebral ischemia-onset protects the brain when ex
167 Tat-N-dimer (3 nmol/g) to mice subjected to focal cerebral ischemia reduces infarct volume with 40%
168 report that the extent of brain injury after focal cerebral ischemia reperfusion is increased, and be
175 HIF-P4H-2 has been shown to be protective in focal cerebral ischemia rodent models, while that of HIF
176 (18)[F]-fluorodeoxyglucose immediately after focal cerebral ischemia showed increased glucose uptake
177 ChRs), as long as 6 hours after the onset of focal cerebral ischemia significantly reduces brain inju
178 rs in JNK-mediated apoptosis after transient focal cerebral ischemia (tFCI), which, when induced by 6
183 used for identifying the ischemic lesion in focal cerebral ischemia, the understanding of spatiotemp
184 cise means of quantitating BBB disruption in focal cerebral ischemia; this method will be of consider
186 tes can be seen chronologically in permanent focal cerebral ischemia using 1H magnetic resonance spec
187 thetic estrogens were examined in a model of focal cerebral ischemia using 210 male, intact female, a
188 g acute stroke interventions in experimental focal cerebral ischemia using endovascular filament midd
189 te and time of administration in relation to focal cerebral ischemia, VEGF can improve histological o
191 er the neuroprotective efficacy of MK-801 in focal cerebral ischemia was dependent on strain and/or v
192 tor knock-out mice, mortality from permanent focal cerebral ischemia was increased, infarct size and
200 Two hours after the end of EA pretreatment, focal cerebral ischemia was induced following 24h reperf
207 ivity following CNS injury, a mouse model of focal cerebral ischemia was utilized to study SHP-1 expr
208 function of TNF from this cellular source in focal cerebral ischemia we used TNF conditional knock ou
209 role of reperfusion in DNA damage following focal cerebral ischemia, we determined the distribution
210 igate its dose dependent effect on permanent focal cerebral ischemia, we examined neurological defici
212 ze and neurological deficits after transient focal cerebral ischemia were more severe, cerebral blood
213 protein nitration, and neuronal death after focal cerebral ischemia were significantly reduced in tr
214 ng pathway for apoptosis following permanent focal cerebral ischemia where there is no reperfusion in
215 ed on observations in vivo that treatment of focal cerebral ischemia with EPO enhances the migration