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1 teractions in both synaptic transmission and brain ischemia.
2  artery occlusive lesions caused hemodynamic brain ischemia.
3 as a model for studying natural tolerance to brain ischemia.
4 he hippocampus and subventricular zone after brain ischemia.
5 pathology of neurological conditions such as brain ischemia.
6 te in apoptotic and necrotic processes after brain ischemia.
7 oxygen-glucose deprivation (OGD) to simulate brain ischemia.
8 dil reduced brain injury in animal models of brain ischemia.
9 roprotective agent in animal models of focal brain ischemia.
10  hippocampal neurons vulnerable to transient brain ischemia.
11 and DNA methylation in vivo after mild focal brain ischemia.
12 , and thrombosis, any of which may result in brain ischemia.
13 a major determinant of cell injury following brain ischemia.
14 x may contribute to neuronal apoptosis after brain ischemia.
15 ning outcome following both global and focal brain ischemia.
16                      Secondary end point was brain ischemia.
17 secondary derangements include posttraumatic brain ischemia.
18 s on the various vascular lesions that cause brain ischemia.
19 neuroprotection in two preclinical models of brain ischemia.
20 alance are key cellular processes altered in brain ischemia.
21 ipal element of the inflammatory response to brain ischemia.
22 rent cell types, including neurons following brain ischemia.
23  microvascular effects that produce critical brain ischemia.
24  potential involvement in recovery following brain ischemia.
25 lization by brain tissue without evidence of brain ischemia.
26 cids may be one potential ligand of TREM2 in brain ischemia.
27 p at 126 days of gestation after exposure to brain ischemia.
28 l death, inflammation and angiogenesis after brain ischemia.
29 angements and cell edema without evidence of brain ischemia.
30 -targeted approach to rescuing neurons after brain ischemia.
31 bstantially to secondary tissue injury after brain ischemia.
32  death of functional neurons after transient brain ischemia.
33  hemodynamic variables and for prevention of brain ischemia.
34 ramidal neurons after recurrent seizures and brain ischemia.
35 in several animal models of global and focal brain ischemia.
36 onal death in a clinically relevant model of brain ischemia.
37 ntegrity of the neurovascular unit following brain ischemia.
38 reases serum levels of S100B, a biomarker of brain ischemia.
39 opioid agonist as efficacious treatments for brain ischemia.
40 cits were significantly worsened after focal brain ischemia.
41 le cerebral artery occlusion (MCAO) model of brain ischemia.
42 opental is neuroprotective in the setting of brain ischemia.
43 neurological conditions such as epilepsy and brain ischemia.
44 dministrations in a mouse model of transient brain ischemia.
45 ctor of the rat hippocampus following global brain ischemia.
46 etuses with and without exposure to in utero brain ischemia.
47 onis 1 (CA1) in an animal model of transient brain ischemia.
48 nd provide a critical overview of reversible brain ischemia.
49 in the cerebral cortex of fetuses exposed to brain ischemia.
50 ransmission in brain and in the pathology of brain ischemia.
51 diated by this pathway in conditions such as brain ischemia.
52 at 1, 2, 3 and 7 days after transient global brain ischemia (12.5 min) in ventilated normothermic rat
53 s are increased in the cerebral cortex after brain ischemia, a condition that induces ER stress.
54 ion inhibition (TI) is observed in transient brain ischemia, a condition that induces persistent TI e
55 nephrine, resulting in a greater severity of brain ischemia after the restoration of spontaneous circ
56                                       During brain ischemia, an excessive release of glutamate trigge
57 were excluded due to extracarotid sources of brain ischemia and 4 were excluded due to carotid occlus
58 cular development and aging and in models of brain ischemia and Alzheimer's disease.
59 PA-mediated brain hemorrhage after transient brain ischemia and embolic stroke in rodents.
60 l target for modulating the glial scar after brain ischemia and facilitating tissue regeneration.
61 hondrial dysfunction appears to occur during brain ischemia and following reperfusion.
62 28+/-0.34 respectively), but severity of the brain ischemia and hence ligand uptake in the lesion app
63    In acidic conditions such as generated by brain ischemia and hypoxia, especially in association wi
64  important role in neuronal cell death after brain ischemia and in late-onset neurodegenerative disea
65 s; such enhancers may be useful for treating brain ischemia and other hypoxic conditions.
66 iochemical and morphologic effects of global brain ischemia and reperfusion following cardiac arrest.
67 eter strategies to treat patients with acute brain ischemia and severe stenosis of intracranial large
68 al intravital microscopy of mice after focal brain ischemia and single neutrophil behavioral analysis
69 of excitotoxic glutamate in animal models of brain ischemia and stroke; however, clinical trials of g
70 TRIF signaling does not confer protection in brain ischemia and suggests the possibility of additiona
71 acterize early BBB disruption in human focal brain ischemia and tested for associations with reperfus
72 e long-term neurological outcome after focal brain ischemia and that the effects may be mediated by a
73 mproves long-term neurological outcome after brain ischemia and the mechanisms for this neuroprotecti
74 bMed, and Google Scholar on terms including "brain ischemia" and "perfusion imaging." The search was
75 % (95% confidence interval, 11.4%-17.1%) for brain ischemia, and 0.7% (95% confidence interval, 0.4%-
76 role in a mouse model of multiple sclerosis, brain ischemia, and Alexander disease.
77 ariety of pathological conditions, including brain ischemia, and cause an acute disruption of synapti
78 athological syndromes such as heart failure, brain ischemia, and stroke.
79  placement tests at 4 days and 4 weeks after brain ischemia, and that infarct volume was increased in
80       We used animal models for experimental brain ischemia as a paradigm of acute brain lesions and
81 8 to 45 years with PFO and no other cause of brain ischemia, as part of the IPSYS registry (Italian P
82 lumes and behavioral deficits after cortical brain ischemia, attenuated cerebral proinflammatory cyto
83 ug with neuroprotective effects in models of brain ischemia attributable to inhibition of brain sodiu
84 ide important insight into the mechanisms of brain ischemia but also demonstrate the complexity of th
85    Cerebral injury may occur not only during brain ischemia but also during reperfusion afterward.
86 peripheral artery disease, had an episode of brain ischemia caused by severe preocclusive carotid art
87                                       Global brain ischemia causes cell death in the CA1 region of th
88                                              Brain ischemia causes oxygen and glucose deprivation (OG
89                We have previously shown that brain ischemia causes rapid dephosphorylation of Kv2.1 s
90           Convincing evidence has shown that brain ischemia causes the proliferation of neural stem c
91 eterious effects can contribute to secondary brain ischemia, cellular death, and neuroinflammation th
92                                        Thus, brain ischemia compromises NK cell-mediated immune defen
93 intracranial large arteries in patients with brain ischemia depend on the extent of infarction, the l
94 sted that rats subjected to transient global brain ischemia develop depressed expression of GluR-B in
95 ) has been implicated in pathologies such as brain ischemia, diabetic peripheral neuropathy, and neur
96                                           In brain ischemia, gating of postsynaptic glutamate recepto
97 levation of intracranial pressure, secondary brain ischemia, herniation, and brain death.
98 itrite exacerbate oxidative DNA damage after brain ischemia.-Huang, D., Shenoy, A., Cui, J., Huang, W
99 optotic and necrotic mechanisms may occur in brain ischemia, immunohistochemical changes of BNIP3 wer
100                          Diabetes influences brain ischemia in a number of different ways.
101 ed CpG oligodeoxynucleotide before transient brain ischemia in mice confers substantial protection ag
102                      Here, we used transient brain ischemia in mice to identify the cellular origin o
103 ion (OGD) in mouse cortical neurons to mimic brain ischemia in neuronal cultures and observed that PA
104 protective effects following transient focal brain ischemia in rats.
105 ees C) after traumatic brain injury or focal brain ischemia in various species.
106 gulated by macrophages/microglia after focal brain ischemia in vivo.
107 [K(+)] ([K(+)](E)) is highly elevated during brain ischemia, in vitro studies aimed at explaining the
108 ension has given way to a focus on secondary brain ischemia, in which cerebral perfusion pressure and
109              Nuclear location of BNIP3 after brain ischemia indicates a novel role for the regulation
110              Here we have determined whether brain ischemia-induced amplification of the NSCs/NPCs in
111                                  The role of brain ischemia-induced NSC/NPC proliferation, however, h
112                                        Acute brain ischemia induces a local neuroinflammatory reactio
113                                              Brain ischemia induces an inflammatory response involvin
114                                        Focal brain ischemia induces inflammation, extracellular matri
115                                              Brain ischemia induces the toxic accumulation of unfolde
116 tly reduced hippocampal neuronal death after brain ischemia, inhibited the ischemia-induced inflammat
117                                              Brain ischemia inhibits immune function systemically, wi
118                                   Reversible brain ischemia is a harbinger for subsequent ischemic st
119 uroprotective therapy.SIGNIFICANCE STATEMENT Brain ischemia is a leading cause of mortality and long-
120  released from membrane phospholipids during brain ischemia is a major source of lipid peroxides.
121 rventional treatment of acute and threatened brain ischemia is a rapidly changing field.
122 e most important predictor of risk following brain ischemia is degree of early clinical reversibility
123  pharmacological treatment with agaphelin in brain ischemia is protective and, regarding its bleeding
124                                              Brain ischemia is responsible for significant morbidity
125                  The function of MANF during brain ischemia is still not known.
126 nary resuscitation model and other models of brain ischemia is that the effects of asphyxic cardiac a
127 est that the upregulation of OPN after focal brain ischemia may play a role in cellular (glia, macrop
128 nvestigated the mechanistic link among acute brain ischemia, microbiota alterations, and the immune r
129 bral ischemia and reperfusion injury in this brain ischemia model.
130                                              Brain ischemia occurs when the blood supply to the brain
131 ffects of DHA in pathological models such as brain ischemia or Alzheimer's disease.
132 ss observed in the striatum following global brain ischemia or in Huntington's disease.
133  (odds ratio [OR], 1.13; 95% CI, 1.02-1.26), brain ischemia (OR, 2.11; 95% CI, 1.58-2.81), brainstem
134                                 In addition, brain ischemia (postmortem exposure) was not associated
135 ly demonstrated that adenosine release after brain ischemia prompts the SVZ to generate new astrocyte
136                                    In global brain ischemia, protective-preservative mild hypothermia
137  of r-Hu-EPO before or up to 6 h after focal brain ischemia reduced injury by approximately 50-75%.
138 ing (2% isoflurane for 30 min at 24 h before brain ischemia) reduced brain infarct sizes and improved
139 cclusion (tMCAO) model was used to establish brain ischemia-reperfusion injury.
140 tive stress contributes to neuronal death in brain ischemia-reperfusion.
141  the SIRT3 role in mitochondrial response to brain ischemia/reperfusion (IR) showed that SIRT3-mediat
142  artery occlusion rat model to emulate human brain ischemia/reperfusion injury in vivo.
143 xamined the role of Tregs after experimental brain ischemia/reperfusion injury.
144 ngly, a robust p53-CypD complex forms during brain ischemia/reperfusion injury.
145 er than anti-leukocyte recruitment following brain ischemia/reperfusion injury.
146                                       In the brain, ischemia/reperfusion (IR) triggered rearrangement
147                                              Brain ischemia results from cardiac arrest, stroke or he
148 al intravital microscopy of mice after focal brain ischemia revealed that neutrophil Cracr2a enhances
149 iac arrest, traumatic brain injury, or focal brain ischemia should be considered for clinical trials.
150 ced neurodegeneration by two models of focal brain ischemia/stroke and by glutamate receptor-mediated
151    To establish whether NOX2 plays a role in brain ischemia, strokes were created in mice, then mice
152                     A brief period of global brain ischemia, such as that induced by cardiac arrest o
153  cellular pathways that link SMC function to brain ischemia susceptibility.
154 lutamate receptors, a condition occurring in brain ischemia that down-regulates GABAB receptors, cons
155 that vascular amyloid contributes to chronic brain ischemia, therefore amyloid burden measured by Pit
156                       During early stages of brain ischemia, transient SMC but not pericyte constrict
157 oxic conditions, which are characteristic of brain ischemia, traumatic brain injury, and neurodegener
158 y is emerging as an important component of a brain ischemia treatment program.
159 trophic factors are neuroprotective and that brain ischemia-triggered NSC/NPC proliferation is crucia
160 LOTBUST trial (Combined Lysis of Thrombus in Brain Ischemia Using Transcranial Ultrasound and Systemi
161                                     Cortical brain ischemia was produced in 16-18 month-old transgeni
162 ell proliferation, for the first 7days after brain ischemia was used to block ischemia-induced NSC/NP
163 impaired written naming of verbs after focal brain ischemia, we combined imaging and behavioral testi
164 In vivo, in rats subjected to thromboembolic brain ischemia, we found that intraischemic helium at 75
165 ink the formation of SGs to TI and DND after brain ischemia, we investigated SG induction in brain re
166       Using a mouse model of transient focal brain ischemia, we report that IL-21 is highly up-regula
167         The rates of the secondary end point brain ischemia were also similar in the 2 treatment grou
168     This contrasts with previous findings in brain ischemia, where Doav and T2 appear to be uncorrela
169                                           In brain ischemia, whether PAR-mediated inhibition of HK-1
170        After traumatic brain injury or focal brain ischemia, which seem to still benefit from even la
171 nt approaches to improve outcome after focal brain ischemia will likely be derived by looking at natu
172 d whether minocycline protects against focal brain ischemia with a wide therapeutic window.
173 udden neurologic dysfunction caused by focal brain ischemia with imaging evidence of acute infarction

 
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