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1 E4 is a risk factor for worse outcomes after brain trauma.
2 ng clot formation and lesion expansion after brain trauma.
3 les in epileptogenesis, memory, learning and brain trauma.
4 entify acute neurodegenerative changes after brain trauma.
5 ological processes and conditions related to brain trauma.
6 jury was unlike that observed for concussive brain trauma.
7 e form of social network interventions after brain trauma.
8  context of the neuropathology of repetitive brain trauma.
9 may impact the injury and repair response to brain trauma.
10 ure, and cortical and hippocampal neurons in brain trauma.
11 on and preserves memory in mice subjected to brain trauma.
12 mpacts may contribute to acute and long-term brain trauma.
13  pathological conditions, such as stroke and brain trauma.
14  of minimally invasive approaches that avoid brain trauma.
15 or contributor to adverse outcomes following brain trauma.
16 a neuroprotective treatment in patients with brain trauma.
17 its best-established epigenetic risk factor, brain trauma.
18  and neuronal damage as secondary effects of brain trauma.
19 , consistent with data from humans following brain trauma.
20 gies to reduce the long-term consequences of brain trauma.
21  formation, and limits neuronal damage after brain trauma.
22 procedures (n = 105) 2 days after concussive brain trauma.
23  development of secondary brain damage after brain trauma.
24 racting the consequences of stroke and acute brain trauma.
25 ine (MA) exacerbate damage induced by severe brain trauma.
26 er peripheral trauma and without evidence of brain trauma.
27  tool in the rehabilitation of patients with brain trauma.
28 ates that control protein turnover following brain trauma.
29 degenerative diseases, cerebral ischemia, or brain trauma.
30 n experimental focal and global ischemia and brain trauma.
31 experimental models of cerebral ischemia and brain trauma.
32 o develop improved treatments for stroke and brain trauma.
33 to develop improved treatment for stroke and brain trauma.
34 stem (CNS) inflammation is involved, such as brain trauma.
35  ERK signaling in the astrocytic response to brain trauma.
36 ng the secondary progression of damage after brain trauma.
37 roversies in experimental animal research on brain trauma.
38 ter injury may prevent epileptogenesis after brain trauma.
39 otential mechanisms of axon reassembly after brain trauma.
40 ons that arise during epilepsy, ischemia and brain trauma.
41 lar surgery (29% [CI, 21% to 33%]), body and brain trauma (29% [CI, 19% to 38%]), and intracranial he
42  astrocytes produced by an in vitro model of brain trauma activates extracellular signal-regulated pr
43 in the community who do not have discernable brain trauma also have subtle prefrontal deficits.
44 hese data suggest a mechanistic link between brain trauma and Abeta levels and the death of neurons.
45         These results are unexpected because brain trauma and chronic illnesses typically cause dimin
46 k of AD associated with previous episodes of brain trauma and for preventing progressive brain amyloi
47 enerative disorders suggests that repetitive brain trauma and hyperphosphorylated tau protein deposit
48  made in the areas of reward and dependence, brain trauma and injury, psychotropic drugs and pain usi
49                In patients with severe acute brain trauma and intracranial hypertension associated wi
50  it to a controlled cortical impact model of brain trauma and measured biochemical, anatomic, and beh
51 cent studies in models of cerebral ischemia, brain trauma and neurodegenerative diseases implicate a
52  response contributes to secondary injury in brain trauma and other disorders.
53 compensates the lost functions after stroke, brain trauma and spinal cord injury.
54 e first to use a calpain inhibitor following brain trauma and suggests that calpain plays a role in t
55 o treat chronic neuronal damage like stroke, brain trauma, and cerebral ischemia.
56 mory deficits, restores motor function after brain trauma, and decreases brain lesion size induced by
57 ological conditions such as ischemic stroke, brain trauma, and epileptic seizures.
58  central nervous system, including epilepsy, brain trauma, and ischemia, likely exacerbates programme
59 ads to excitotoxic neuronal death in stroke, brain trauma, and neurodegenerative disorders.
60 l vascular disease of diabetic origin, blunt brain trauma, and rheumatoid joints and in an animal mod
61 nial pressure (ICP) caused by brain surgery, brain trauma, and severe stroke.
62 gressive diseases in adults, such as stroke, brain trauma, and spinal cord injury.
63 schemic stroke, subarachnoid hemorrhage, and brain trauma, and suggest a novel application for contin
64 h younger age, longer time since injury, and brain trauma as an etiologic factor.
65 stem to the challenges imposed by the WD and brain trauma as evidenced by results showing that the WD
66 es: one with severe epilepsy following focal brain trauma at 17 weeks gestation, one with hemimegalen
67 juries (including cerebrovascular accidents, brain trauma, brain tumors, and demyelinating disorders)
68 ropsychiatric diseases as well as stroke and brain trauma by genesis of new neurons and their incorpo
69 I) device inflicts mild, moderate, or severe brain trauma by precise compression of the head using a
70 , VIP prevents neuronal cell death following brain trauma by reducing the inflammatory response of ne
71                                              Brain trauma by use of a controlled cortical impact devi
72 tic aneurysm) exsanguination, without severe brain trauma, by enabling evacuation and resuscitative s
73 filaments in CTE and the mechanisms by which brain trauma can lead to their formation are unknown.
74 g neurodegenerative diseases and explore how brain trauma can serve as a disease initiator or acceler
75 mental mouse model of TBI that mild forms of brain trauma cause severe deficits in meningeal lymphati
76 ntation before and after cold injury-induced brain trauma (CIBT) in mice, in which apoptosis is assum
77 lved in many neurological diseases including brain trauma, epilepsies, autism and schizophrenia.
78 ure monitors in >50% of patients meeting the Brain Trauma Foundation criteria for intracranial pressu
79 ation between hospital-level compliance with Brain Trauma Foundation guidelines and mortality rates a
80                Patients with TBI who met the Brain Trauma Foundation guidelines for ICP monitoring we
81 lity rate and hospital-level compliance with Brain Trauma Foundation guidelines for intracranial pres
82                              Despite current Brain Trauma Foundation guidelines, ICP monitoring is us
83  patients who received care according to the Brain Trauma Foundation guidelines; and c) to correlate
84                                          The Brain Trauma Foundation has revised perfusion pressure t
85 t the monitoring criteria recommended by the Brain Trauma Foundation.
86 -80 years) at least 6 months after stroke or brain trauma from 34 neurology or rehabilitation clinics
87 the 1-month survival rate of mice with acute brain trauma from 50 to 90% and promote the recovery of
88                        Delayed cooling after brain trauma has also been effective in a subgroup of ad
89 oping epilepsy and seizures following severe brain trauma has been shown to increase with age.
90       Cognitive losses resulting from severe brain trauma have long been associated with the focal re
91 Abeta) have been found within days following brain trauma in humans, similar to the hallmark plaque p
92 ed at 6, 24 and 72 h following non-contusive brain trauma in the 17 day-old rat to examine the causal
93                      We developed a model of brain trauma in transgenic mice that overexpress mutant
94 ients who are aging or with dementia or mild brain trauma; increased conspicuity of superficial sider
95                                     Although brain trauma is a risk factor for Alzheimer's disease, n
96                                              Brain trauma is associated with long-term decrements in
97 teral cortex in the recovery from unilateral brain trauma is not limited to the regions homologous to
98 lthough axonal injury is a common feature of brain trauma, little is known of the immediate morpholog
99 lem in many types of brain injuries, such as brain trauma, localized brain edema, hematoma, focal cer
100 at increases in NO formation observed during brain trauma may contribute to disruption of the blood-b
101 FICANCE STATEMENT: During ischemic stroke or brain trauma, mitochondria can either protect neurons by
102 ts in preclinical models of ischemic stroke, brain trauma, multiple sclerosis, amyotrophic lateral sc
103 ocial factors may also modify the effects of brain trauma on clinical and pathological outcomes.
104 for restoring brain function in the event of brain trauma or disease.
105 , and risk factors (hypertension, history of brain trauma or intracranial vascular malformations).
106 g of therapeutic approaches in patients with brain traumas or neurodegenerative disorders and preserv
107 ve impairments in the absence of traditional brain trauma pathology, and transcriptomic profiling of
108 NT A recent clinical study showed that human brain trauma patients had enhanced expression of type-1
109 as a novel mechanism of injury in stroke and brain trauma patients.
110 comes associated with exposure to repetitive brain trauma (RBT) continues to strengthen.
111 sment of these conditions following subtotal brain trauma requires a comprehensive understanding of t
112 preserve motor and cognitive function in the brain trauma setting is unknown.
113  that clinical evaluation of the severity of brain trauma should take into account the spatial patter
114 vior unrelated to genetic manipulation or to brain trauma.SIGNIFICANCE STATEMENT Our evidence that in
115 for treating the deleterious consequences of brain trauma; this is in part due to a lack of complete
116 tability may be a key mechanism linking mild brain trauma to chronic degeneration.
117               Research challenges concerning brain trauma, uncontrolled hemorrhagic shock, and "suspe
118  the CRS-R within 28 days after injury), and brain trauma was an etiologic factor in 50%.
119                                              Brain trauma was clinically associated with increased os
120 enumbral-type depolarizations occur in human brain trauma, we analysed electrocorticographic recordin
121  avian tectal model of penetrating embryonic brain trauma, without confounding maternal and sibling e

 
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