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1 pathological conditions, such as stroke and brain trauma.
2 of minimally invasive approaches that avoid brain trauma.
3 or contributor to adverse outcomes following brain trauma.
4 a neuroprotective treatment in patients with brain trauma.
5 and neuronal damage as secondary effects of brain trauma.
6 , consistent with data from humans following brain trauma.
7 gies to reduce the long-term consequences of brain trauma.
8 formation, and limits neuronal damage after brain trauma.
9 procedures (n = 105) 2 days after concussive brain trauma.
10 development of secondary brain damage after brain trauma.
11 ure, and cortical and hippocampal neurons in brain trauma.
12 racting the consequences of stroke and acute brain trauma.
13 ine (MA) exacerbate damage induced by severe brain trauma.
14 er peripheral trauma and without evidence of brain trauma.
15 ates that control protein turnover following brain trauma.
16 on and preserves memory in mice subjected to brain trauma.
17 degenerative diseases, cerebral ischemia, or brain trauma.
18 n experimental focal and global ischemia and brain trauma.
19 experimental models of cerebral ischemia and brain trauma.
20 mpacts may contribute to acute and long-term brain trauma.
21 o develop improved treatments for stroke and brain trauma.
22 to develop improved treatment for stroke and brain trauma.
23 stem (CNS) inflammation is involved, such as brain trauma.
24 ERK signaling in the astrocytic response to brain trauma.
25 ng the secondary progression of damage after brain trauma.
26 roversies in experimental animal research on brain trauma.
27 otential mechanisms of axon reassembly after brain trauma.
28 ons that arise during epilepsy, ischemia and brain trauma.
29 les in epileptogenesis, memory, learning and brain trauma.
30 entify acute neurodegenerative changes after brain trauma.
31 lar surgery (29% [CI, 21% to 33%]), body and brain trauma (29% [CI, 19% to 38%]), and intracranial he
32 astrocytes produced by an in vitro model of brain trauma activates extracellular signal-regulated pr
34 hese data suggest a mechanistic link between brain trauma and Abeta levels and the death of neurons.
35 k of AD associated with previous episodes of brain trauma and for preventing progressive brain amyloi
36 enerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposit
37 made in the areas of reward and dependence, brain trauma and injury, psychotropic drugs and pain usi
39 it to a controlled cortical impact model of brain trauma and measured biochemical, anatomic, and beh
40 cent studies in models of cerebral ischemia, brain trauma and neurodegenerative diseases implicate a
43 e first to use a calpain inhibitor following brain trauma and suggests that calpain plays a role in t
44 mory deficits, restores motor function after brain trauma, and decreases brain lesion size induced by
46 central nervous system, including epilepsy, brain trauma, and ischemia, likely exacerbates programme
48 l vascular disease of diabetic origin, blunt brain trauma, and rheumatoid joints and in an animal mod
51 schemic stroke, subarachnoid hemorrhage, and brain trauma, and suggest a novel application for contin
52 stem to the challenges imposed by the WD and brain trauma as evidenced by results showing that the WD
53 es: one with severe epilepsy following focal brain trauma at 17 weeks gestation, one with hemimegalen
54 juries (including cerebrovascular accidents, brain trauma, brain tumors, and demyelinating disorders)
55 , VIP prevents neuronal cell death following brain trauma by reducing the inflammatory response of ne
57 tic aneurysm) exsanguination, without severe brain trauma, by enabling evacuation and resuscitative s
58 ntation before and after cold injury-induced brain trauma (CIBT) in mice, in which apoptosis is assum
60 ure monitors in >50% of patients meeting the Brain Trauma Foundation criteria for intracranial pressu
61 ation between hospital-level compliance with Brain Trauma Foundation guidelines and mortality rates a
62 lity rate and hospital-level compliance with Brain Trauma Foundation guidelines for intracranial pres
64 patients who received care according to the Brain Trauma Foundation guidelines; and c) to correlate
67 -80 years) at least 6 months after stroke or brain trauma from 34 neurology or rehabilitation clinics
70 Abeta) have been found within days following brain trauma in humans, similar to the hallmark plaque p
71 ed at 6, 24 and 72 h following non-contusive brain trauma in the 17 day-old rat to examine the causal
75 teral cortex in the recovery from unilateral brain trauma is not limited to the regions homologous to
76 lthough axonal injury is a common feature of brain trauma, little is known of the immediate morpholog
77 lem in many types of brain injuries, such as brain trauma, localized brain edema, hematoma, focal cer
78 at increases in NO formation observed during brain trauma may contribute to disruption of the blood-b
79 FICANCE STATEMENT: During ischemic stroke or brain trauma, mitochondria can either protect neurons by
80 ts in preclinical models of ischemic stroke, brain trauma, multiple sclerosis, amyotrophic lateral sc
81 g of therapeutic approaches in patients with brain traumas or neurodegenerative disorders and preserv
84 sment of these conditions following subtotal brain trauma requires a comprehensive understanding of t
86 that clinical evaluation of the severity of brain trauma should take into account the spatial patter
87 vior unrelated to genetic manipulation or to brain trauma.SIGNIFICANCE STATEMENT Our evidence that in
89 enumbral-type depolarizations occur in human brain trauma, we analysed electrocorticographic recordin
90 avian tectal model of penetrating embryonic brain trauma, without confounding maternal and sibling e
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