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1 anges in extracranial organs can occur after acute brain injury.
2  membrane oxygenation nonsurvivors developed acute brain injury.
3 unresponsive patients (aged >=18 years) with acute brain injury.
4 a paucity of data on other clinical types of acute brain injury.
5 for neurological outcome and mortality after acute brain injury.
6 d improve clinical outcomes in patients with acute brain injury.
7 ntilator-free days among adult patients with acute brain injury.
8  and nurses of patients admitted with severe acute brain injury.
9 oagulation disturbances were associated with acute brain injury.
10  hepatic impairment were not associated with acute brain injury.
11 he risk of cerebral edema and ischemia after acute brain injury.
12  treating TBI and potentially other forms of acute brain injury.
13  extracellular K(+) levels in the setting of acute brain injury.
14  outcomes of patients with severe non-anoxic acute brain injury.
15 predicting time to recovery in patients with acute brain injury.
16 o characterize the immune response to severe acute brain injury.
17 nts in a consecutive series of patients with acute brain injury.
18 at TGF-beta1 may be a therapeutic target for acute brain injury.
19 ectroencephalographic (EEG) recordings after acute brain injury.
20 in vivo phage display screening in mice with acute brain injury.
21 e microbiota has an impact on the outcome of acute brain injury.
22 eful in cell-free therapeutic approaches for acute brain injury.
23  target therapeutically in the management of acute brain injury.
24 of conscious level, the clinical hallmark of acute brain injury.
25  candidate target for advanced monitoring in acute brain injury.
26 the physiological response to seizures after acute brain injury.
27  also augment aspects of inflammation during acute brain injury.
28 testinal bleed, acute coronary syndrome, and acute brain injury.
29  to minimize the inflammatory response after acute brain injury.
30 going invasive intracranial monitoring after acute brain injury.
31 resent an important local source of C3 after acute brain injury.
32 h apolipoprotein E affects outcome following acute brain injury.
33 cranial pressure and fatal outcome following acute brain injury.
34  with those of normothermia in patients with acute brain injury.
35 contributes to secondary neuronal loss after acute brain injury.
36 n-caspase-dependent neuronal death following acute brain injury.
37 te to the progression of tissue damage after acute brain injury.
38 (Coma Recovery Scale-Revised) 3 months after acute brain injury.
39 egree of neurologic insult in children after acute brain injury.
40 disorders of consciousness caused by severe, acute brain injury.
41  Organization registry, approximately 5% had acute brain injury.
42 s are commonly administered to patients with acute brain injury.
43 related well with qualitative MRI scoring of acute brain injury.
44  Critically ill patients are at high risk of acute brain injury.
45 ry of therapeutics in clinical management of acute brain injuries.
46 he brain is implicated in the progression of acute brain injuries.
47                           Early detection of acute brain injury (ABI) at the bedside is critical in i
48                          We aimed to compare acute brain injury (ABI) frequency, thrombotic, and hemo
49                                              Acute brain injury (ABI) included hypoxic-ischemic brain
50 strategies between patients with and without acute brain injury (ABI) remain incompletely characteriz
51 CP) is the standard of care in patients with acute brain injury (ABI) with impaired consciousness.
52 genation (ECMO), it may also amplify risk of acute brain injury (ABI).
53 ter than or equal to 80% adult patients with acute brain injury admitted to the ICU and mechanically
54               One in four patients developed acute brain injury after extracorporeal cardiopulmonary
55       Only eight patients (32%) were without acute brain injury after extracorporeal membrane oxygena
56  the relationship between MMP-9 activity and acute brain injury after ICH is not determined.
57                                Mechanisms of acute brain injury after ICH remain to be clarified.
58  a therapeutic strategy for the treatment of acute brain injury after ICH.
59                                    Following acute brain injury, albumin may gain access to the brain
60  incompletely utilized information regarding acute brain injuries and neurologic outcomes.
61                                Patients with acute brain injury and anemia randomized to a liberal tr
62                       Anemia is common after acute brain injury and can be associated with brain tiss
63 ntially a novel neuroprotective approach for acute brain injury and chronic neurodegenerative disorde
64                     Thus, in addition to the acute brain injury and consequent impairment, ischemic s
65 preting patterns of brain activity following acute brain injury and has profound implications for cli
66 lsive seizures (NCSz) are frequent following acute brain injury and have been implicated as a cause o
67 Sept 30, 2021, we screened 598 patients with acute brain injury and included 193 (32%) patients, of w
68 chanism, timing, and effective monitoring of acute brain injury and its management is necessary.
69 l fluid [Mg] is largely maintained following acute brain injury and limits the brain bioavailability
70 sive cellular depolarization associated with acute brain injury and migraine aura.
71 ficial or harmful when used in patients with acute brain injury and raised intracranial pressure.
72                  The review encompassed both acute brain injury and systemic critical illness conditi
73 l pressure (ICP) monitoring in patients with acute brain injury and the effects of ICP on patients' o
74  during normal ageing, neurodegeneration and acute brain injuries, and how prolonged BBB impairment a
75 kdown of electrochemical gradients following acute brain injury, and also elicits dynamic changes in
76          Although traumatic and haemorrhagic acute brain injury are generally considered separately,
77 ies of clinically unresponsive patients with acute brain injury are largely uncertain.
78 rebral physiologic effects of seizures after acute brain injury are poorly understood.
79 of injury suggesting that patients sustained acute brain injury as a consequence of cardiogenic shock
80 ts with hemorrhagic stroke and perhaps other acute brain injuries associated with cell death by apopt
81 t ICP monitoring practises for patients with acute brain injury at centres around the world and to as
82  Purpose To evaluate quantitative volumes of acute brain injury at MRI in neonates with hypoxic ische
83 ; 235 male) and 113 (27%) showed evidence of acute brain injury at MRI.
84 s have never been conducted in patients with acute brain injuries because of concerns about carbon di
85 t difference was seen in the rate of overall acute brain injury between venoarterial extracorporeal m
86 s generated by neuroradiologists at the Yale Acute Brain Injury Biorepository.
87 ons are inherently associated with a risk of acute brain injury, both periprocedurally and postproced
88 sults have suggested a role for autophagy in acute brain injury but an involvement in subarachnoid he
89  lesion development and worse outcomes after acute brain injury, but accurate diagnosis by neurophysi
90 y of behaviorally unresponsive patients with acute brain injury, but acquisition and analysis of task
91 are associated with worse outcomes following acute brain injury, but their effect on long-term clinic
92 ic action to provide neuroprotection against acute brain injury, but these agents can also cause toxi
93 venues of investigation for the detection of acute brain injury by neuroimaging, in addition to preve
94 n the prevention, diagnosis and treatment of acute brain injury caused by cardiovascular intervention
95 cognitive deficits, resembling delirium, and acute brain injury contributing to long-term cognitive i
96                                    Volume of acute brain injury, defined as brain with apparent diffu
97 atients, 812 (5.1%) had at least one type of acute brain injury, defined as ischemic stroke, hemorrha
98                          In a mouse model of acute brain injury, DPTIP released from P18 significantl
99 der who were admitted to the ICU with either acute brain injury due to primary haemorrhagic stroke (i
100 e not provided definitive direct evidence of acute brain injury during a HD treatment session.
101                                     Reported acute brain injury during venoarterial extracorporeal me
102 ting ventilatory strategies in patients with acute brain injuries, especially those with lung damage,
103 hird behaviorally unresponsive patient after acute brain injury, frequently precede detection of CMD
104 ) NLP model to extract and summarize data on acute brain injuries from head CT reports.
105 ents in a single intensive care unit who had acute brain injury from a variety of causes and who were
106 ated active caspases in astrocytes following acute brain injury, here we present evidence functionall
107  facilitate early detection and treatment of acute brain injury in critical care.
108 erize the types, timing, and risk factors of acute brain injury in extracorporeal membrane oxygenatio
109  of neurologically ill adults or adults with acute brain injury in ICUs.
110 udies lack information on characteristics of acute brain injury in patients with extracorporeal membr
111 itoring is necessary to define the timing of acute brain injury in patients with extracorporeal membr
112      Despite a decrease in the prevalence of acute brain injury in recent years, mortality rates rema
113            Affected children commonly suffer acute brain injury in the context of a catabolic state a
114 S, produces both working-memory deficits and acute brain injury in the degenerating brain and that th
115                         The risk factors for acute brain injury included hypertension history (11 vs
116 uid management is important in patients with acute brain injury, including subarachnoid hemorrhage.
117                     Here we demonstrate that acute brain injury induces vascular damage, meningeal ce
118             Improving the prognostication of acute brain injury is a key element of critical care.
119                                     Although acute brain injury is common in patients receiving extra
120 e oxygenation risk factors and the timing of acute brain injury is necessary to develop appropriate p
121 ith clinical benefits in adult patients with acute brain injury is unknown.
122 PDs, suggesting that additional damage after acute brain injury may be reflected by frequency changes
123 SIGNIFICANCE STATEMENT In in vitro models of acute brain injury, microglial phagocytosis is overwhelm
124                                              Acute brain injury mobilizes circulating leukocytes to t
125                      Six months after severe acute brain injury, most patients survived to a state th
126 ed in consecutive unresponsive patients with acute brain injury (n = 107) who underwent EEG-based CMD
127         Treatment decisions following severe acute brain injury need to consider patients' goals-of-c
128 to gain a greater understanding of p75NTR in acute brain injuries, neurodegenerative diseases and gen
129                        In in vitro models of acute brain injury, neuronal death may overwhelm the cap
130 ole of endogenous apolipoprotein E following acute brain injury, noninvasive magnetic resonance imagi
131 c inflammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mech
132 ns such as acute symptomatic seizures due to acute brain injury or metabolic derangements, or unprovo
133 gic processes associated with seizures after acute brain injury previously described in laboratory ex
134  study suggest that for patients with severe acute brain injury, prognosis discordance between physic
135                  However, for most causes of acute brain injury, prognostic models are not sufficient
136           Among critically ill patients with acute brain injury, prophylactic IV antibiotics were ass
137 hered head CT reports to expand knowledge of acute brain injury radiographic phenotypes.
138 tor-free days (up to 28 d) among adults with acute brain injury receiving invasive mechanical ventila
139  future directions in clinical research into acute brain injury related to cardiovascular interventio
140 uidelines generally do not cover the area of acute brain injury related to cardiovascular invasive pr
141                        The great majority of acute brain injury results from trauma or from disorders
142       Family members of patients with severe acute brain injury (SABI) are at risk for poor psycholog
143                         Patients with severe acute brain injury (SABI) are unable to make their own d
144                 In the early phase of severe acute brain injury (SABI), surrogate decision-makers mus
145                         Thirty patients with acute brain injury secondary to subarachnoid hemorrhage,
146 ardiopulmonary resuscitation or other severe acute brain injuries should be deferred for >/=24 hrs if
147 ardiopulmonary resuscitation or other severe acute brain injuries should be deferred for 24 hours or
148 non-transgenic littermates, in two models of acute brain injury: stroke caused by middle cerebral art
149                                 The National Acute Brain Injury Study: Hypothermia II (NABIS: H II) w
150 ribute to neurotoxicity, particularly during acute brain injuries, such as cerebral ischemia, trauma,
151 duces ER stress and provides protection from acute brain injury, suggesting that strategies for enhan
152 hat the BrainNERD model accurately extracted acute brain injury terms and their properties from head
153              Identifying blood biomarkers of acute brain injury that are associated with future NCI c
154 ein E (apoE) plays a role in the response to acute brain injury, the mechanisms as yet remain unknown
155                     For patients with severe acute brain injury, the objective of this study was to b
156 he early myofibroblast state exacerbated sub-acute brain injury, tissue loss and secondary neuroinfla
157 ment is common across critical illness, from acute brain injury to systemic conditions like sepsis, c
158 f an otherwise epileptogenesis-precipitating acute brain injury, transgenic mice with reduced forebra
159         The correlation between quantitative acute brain injury volume and qualitative MRI scores was
160                                       Severe acute brain injury was defined as stroke, traumatic brai
161                              The most common acute brain injury was hypoxic-ischemic brain injury (44
162 orted postmortem neuropathological findings, acute brain injury was noted in 47% of patients.
163 mporary, multicenter cohort of patients with acute brain injury, we found no association between the
164 lled clinical trial, 190 adult patients with acute brain injury were assigned to receive either a lun
165 t admitted to the ICU or with other forms of acute brain injury were excluded from the study.
166 lower Spo2 target had a higher prevalence of acute brain injury, whereas patients predicted to benefi
167  mechanically ventilated adult patients with acute brain injury who had a first successful spontaneou
168                            All patients with acute brain injury who were monitored with brain tissue
169       In unconscious appearing patients with acute brain injury, wilful brain activation to motor com
170  the presence and volume (in milliliters) of acute brain injury with 24-month outcomes were evaluated
171 y analysis of the Outcome Prognostication of Acute Brain Injury With the Neurological Pupil Index (OR
172 ndred fifty-two critically ill patients with acute brain injury, with a median age of 54 years, of wh
173 ce that MMP-9 may play a deleterious role in acute brain injury within the first 3 days after ICH.
174                Conclusions: In patients with acute brain injury without ARDS, a lung-protective venti

 
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