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1 at TGF-beta1 may be a therapeutic target for acute brain injury.
2 target therapeutically in the management of acute brain injury.
3 of conscious level, the clinical hallmark of acute brain injury.
4 candidate target for advanced monitoring in acute brain injury.
5 ectroencephalographic (EEG) recordings after acute brain injury.
6 the physiological response to seizures after acute brain injury.
7 also augment aspects of inflammation during acute brain injury.
8 testinal bleed, acute coronary syndrome, and acute brain injury.
9 to minimize the inflammatory response after acute brain injury.
10 going invasive intracranial monitoring after acute brain injury.
11 resent an important local source of C3 after acute brain injury.
12 h apolipoprotein E affects outcome following acute brain injury.
13 in vivo phage display screening in mice with acute brain injury.
14 cranial pressure and fatal outcome following acute brain injury.
15 with those of normothermia in patients with acute brain injury.
16 contributes to secondary neuronal loss after acute brain injury.
17 n-caspase-dependent neuronal death following acute brain injury.
18 te to the progression of tissue damage after acute brain injury.
19 egree of neurologic insult in children after acute brain injury.
20 e microbiota has an impact on the outcome of acute brain injury.
21 eful in cell-free therapeutic approaches for acute brain injury.
22 ry of therapeutics in clinical management of acute brain injuries.
23 he brain is implicated in the progression of acute brain injuries.
28 ntially a novel neuroprotective approach for acute brain injury and chronic neurodegenerative disorde
30 preting patterns of brain activity following acute brain injury and has profound implications for cli
31 lsive seizures (NCSz) are frequent following acute brain injury and have been implicated as a cause o
32 l fluid [Mg] is largely maintained following acute brain injury and limits the brain bioavailability
33 ficial or harmful when used in patients with acute brain injury and raised intracranial pressure.
34 kdown of electrochemical gradients following acute brain injury, and also elicits dynamic changes in
37 ts with hemorrhagic stroke and perhaps other acute brain injuries associated with cell death by apopt
38 sults have suggested a role for autophagy in acute brain injury but an involvement in subarachnoid he
39 ic action to provide neuroprotection against acute brain injury, but these agents can also cause toxi
40 ated active caspases in astrocytes following acute brain injury, here we present evidence functionall
43 PDs, suggesting that additional damage after acute brain injury may be reflected by frequency changes
44 ole of endogenous apolipoprotein E following acute brain injury, noninvasive magnetic resonance imagi
45 ns such as acute symptomatic seizures due to acute brain injury or metabolic derangements, or unprovo
46 gic processes associated with seizures after acute brain injury previously described in laboratory ex
50 ardiopulmonary resuscitation or other severe acute brain injuries should be deferred for >/=24 hrs if
51 ardiopulmonary resuscitation or other severe acute brain injuries should be deferred for 24 hours or
52 non-transgenic littermates, in two models of acute brain injury: stroke caused by middle cerebral art
54 ribute to neurotoxicity, particularly during acute brain injuries, such as cerebral ischemia, trauma,
55 duces ER stress and provides protection from acute brain injury, suggesting that strategies for enhan
56 ein E (apoE) plays a role in the response to acute brain injury, the mechanisms as yet remain unknown
57 f an otherwise epileptogenesis-precipitating acute brain injury, transgenic mice with reduced forebra
58 ce that MMP-9 may play a deleterious role in acute brain injury within the first 3 days after ICH.
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