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1   Ca2+ toxicity remains the central focus of ischemic brain injury.
2 of various neurological disorders, including ischemic brain injury.
3 ces an inflammatory response and exacerbates ischemic brain injury.
4 tiated oligodendrocytes in perinatal hypoxic/ischemic brain injury.
5 damage in a rodent model of neonatal hypoxic-ischemic brain injury.
6 itation and the most common type was hypoxic-ischemic brain injury.
7        Reactive oxygen species contribute to ischemic brain injury.
8  evidence against a role for inflammation in ischemic brain injury.
9 of biliverdin reductase (BVR) in response to ischemic brain injury.
10 cidosis is considered to be a contributor to ischemic brain injury.
11 rtant in determining the extent of anoxic or ischemic brain injury.
12 onged role for apoptosis in neonatal hypoxic ischemic brain injury.
13 ontributes to poor tissue outcome after mild ischemic brain injury.
14  and apoptosis, processes that contribute to ischemic brain injury.
15 ell death by influencing bcl-2 expression in ischemic brain injury.
16 nce suggesting that apoptosis is involved in ischemic brain injury.
17 recognized factor by which NO contributes to ischemic brain injury.
18 tion products contribute to the evolution of ischemic brain injury.
19 receptor antagonist protein (IL-1ra) reduces ischemic brain injury.
20 specifically at the secondary progression of ischemic brain injury.
21 pletion occurs with other insults, including ischemic brain injury.
22 d to capture the imaging severity of hypoxic ischemic brain injury.
23 al models of neurodegenerative diseases, and ischemic brain injury.
24 ic cardiac arrest are chiefly due to hypoxic-ischemic brain injury.
25 dysfunction and a donor neonate with hypoxic-ischemic brain injury.
26 fide accumulation, bioenergetic failure, and ischemic brain injury.
27 omic datasets from different mouse models of ischemic brain injury.
28 d the most common cause of death was hypoxic-ischemic brain injury.
29 ypoxia and identify a therapeutic target for ischemic brain injury.
30 ulate ASIC1 and to reduce the progression of ischemic brain injury.
31 ation, propagation, and resolution phases of ischemic brain injury.
32 that interferes with neuronal cell death and ischemic brain injury.
33  modification are linked to the pathology of ischemic brain injury.
34 tosides, is implicated in protection against ischemic brain injury.
35 ity represents a major cellular component of ischemic brain injury.
36 marker for the severity of perinatal hypoxic-ischemic brain injury.
37  Cerebral edema is a serious complication of ischemic brain injury.
38  effects of circulating monocytes in hypoxic-ischemic brain injury.
39 gnaling in a mouse model of neonatal hypoxic-ischemic brain injury.
40 tor (TLR) signaling after a neonatal hypoxic-ischemic brain injury.
41 signaling pathway, which plays a key role in ischemic brain injury.
42 , providing a novel therapeutic strategy for ischemic brain injury.
43  potentially important therapeutic target in ischemic brain injury.
44 ed clinical improvement often observed after ischemic brain injury.
45 r modulation of NADPH oxidase activity after ischemic brain injury.
46 imately lead to viable treatment options for ischemic brain injury.
47  examine the protective effect of MANF after ischemic brain injury.
48  deficiency plays a critical role in hypoxic-ischemic brain injury.
49 d AP neuroprotection following traumatic and ischemic brain injury.
50 t excitotoxicity contribute significantly to ischemic brain injury.
51 ms employed by NRG-1 to protect neurons from ischemic brain injury.
52 hanism by which hyperglycemia can exacerbate ischemic brain injury.
53 latile anesthetics have been shown to reduce ischemic brain injury.
54 ain neurons, and appears to modulate hypoxic-ischemic brain injury.
55 tion may be a valuable strategy for treating ischemic brain injury.
56 1 cluster is involved in the pathogenesis of ischemic brain injury.
57 o estradiol-mediated neuroprotection against ischemic brain injury.
58 which can lead to brain edema and exacerbate ischemic brain injury.
59  into clinically useful treatments to reduce ischemic brain injury.
60 hemic stroke (10% vs 1%; p < 0.001), hypoxic-ischemic brain injury (13% vs 1%; p < 0.001), and brain
61  by intracranial hemorrhage (6%) and hypoxic-ischemic brain injury (4%).
62 e most common acute brain injury was hypoxic-ischemic brain injury (44%), followed by intracranial he
63 mplication, 23% (95% CI, 0.14-0.32%) hypoxic-ischemic brain injury, 6% (95% CI, 0.02-0.11%) ischemic
64 hemic stroke (10% vs 1%; p < 0.001), hypoxic-ischemic brain injury (7% vs 1%; p = 0.02), and brain de
65 le encephalopathy syndrome (9%), and hypoxic-ischemic brain injury (7%).
66  proven neuroprotective treatment exists for ischemic brain injury after cardiac arrest.
67                      Inflammation can extend ischemic brain injury and adversely affect outcome in ex
68 brain injury at MRI in neonates with hypoxic ischemic brain injury and correlate these findings with
69 y, an important factor in the development of ischemic brain injury and edema formation.
70 nd histidine, is robustly neuroprotective in ischemic brain injury and has a wide clinically relevant
71 ells or brain resident cells, contributes to ischemic brain injury and hemorrhage.
72 ppresses neurovascular remodeling, increases ischemic brain injury and impairs functional recovery at
73               Inhibition of GSNOR attenuated ischemic brain injury and improved survival in wild-type
74 ition or genetic deletion of GSNOR prevented ischemic brain injury and improved survival rates by res
75 cerebral ischemia-reperfusion contributes to ischemic brain injury and is a potential therapeutic tar
76 eptor (A(2A)R) consistently protects against ischemic brain injury and other neural insults, but the
77 the neuroprotective effect of Bcl-xL against ischemic brain injury and provide the first evidence tha
78 ults support the functional role of MCP-1 in ischemic brain injury and reveal a distinct temporal and
79 in the genetic variability in sensitivity to ischemic brain injury and stroke outcome.
80 e involvement of MAP kinase pathway in focal ischemic brain injury and suggest that this effect might
81 ascade in BMDCs is an important modulator of ischemic brain injury and that ischemic brain and liver
82   We conclude that G-CSF ameliorates hypoxic-ischemic brain injury and that this may occur in part by
83 r role for complement-mediated cell death in ischemic brain injury and the prospect of using IVIG in
84 he mechanisms of neuronal survival following ischemic brain injury and to the development of therapeu
85 y provide insight into mechanisms of hypoxic-ischemic brain injury and, hence, recovery.
86 rebral ischemia (ischemic infarct or hypoxic ischemic brain injury) and intracranial hemorrhage (intr
87 ve impairment, including multiple sclerosis, ischemic brain injury, and Alzheimer's disease.
88 s of age and energy intake on the outcome of ischemic brain injury, and elucidated the underlying mec
89        Zn(2+) is an important contributor to ischemic brain injury, and recent studies support the hy
90   Hypothermia (32-34 degrees C) can mitigate ischemic brain injury, and some evidence suggests that i
91 city, a critical factor in the initiation of ischemic brain injury, and to abrogation of the deleteri
92         Episodes of brain hypoxia in hypoxic ischemic brain injury are frequent, and perfusion within
93              Irregular, sporadic episodes of ischemic brain injury are known to occur in sickle cell
94 nation of brain death; patients with hypoxic-ischemic brain injury are more likely to undergo ancilla
95 r improving outcome in patients with hypoxic-ischemic brain injury as a result of cardiac arrest is w
96 at potential as a therapeutic agent in focal ischemic brain injury, as exogenous beta-estradiol has p
97 BDNF also markedly protected against hypoxic-ischemic brain injury at PD7.
98 Extracellular adenosine critically modulates ischemic brain injury, at least in part through activati
99 f cerebral damage after acute global hypoxic-ischemic brain injury but, thus far, these putative neur
100 poxygenase (12/15-LOX), which contributes to ischemic brain injury, but its human and rodent isozymes
101 eceptor CD36 is a critical factor initiating ischemic brain injury, but the cell type(s) expressing C
102  inducible NO synthase (iNOS) contributes to ischemic brain injury, but the cell types expressing iNO
103      Macrophages are viewed as amplifiers of ischemic brain injury, but the origin of injury-producin
104 ic acid, is thought to contribute to hypoxic-ischemic brain injury by generating oxygen-free radicals
105                                              Ischemic brain injury causes local inflammation, which i
106           There were 4 deaths resulting from ischemic brain injury, chronic rejection, biliary sepsis
107 The development of new therapies for hypoxic-ischemic brain injury depends on such understanding.
108               In patients at risk of hypoxic ischemic brain injury following cardiac arrest, we sough
109                                 During early ischemic brain injury, glutamate receptor hyperactivatio
110                        Patients with hypoxic-ischemic brain injury had more hypertension (8 vs 4; p =
111                  A role of p38 MAP kinase in ischemic brain injury has been previously suggested by p
112 ents with cardiac arrest who develop hypoxic ischemic brain injury (HIBI) after return of spontaneous
113                             Neonatal hypoxic-ischemic brain injury (HIBI) results in part from excess
114 s based on the type of brain injury: hypoxic-ischemic brain injury (HIBI) vs. non-HIBI.
115                                           In ischemic brain injury, however, activation of this Ca(2+
116 donors, intracranial bleed in 24, and anoxic/ischemic brain injury in 26.
117 tudy, we demonstrated the effects of EPCs on ischemic brain injury in a mouse model of transient midd
118 d-type bone marrow cells) largely reinstates ischemic brain injury in global A(2A)R knockout mice.
119  a novel therapeutic agent for inhibition of ischemic brain injury in humans.
120     We investigated whether the reduction in ischemic brain injury in inducible nitric oxide synthase
121 d alterations in the intestinal flora reduce ischemic brain injury in mice, an effect transmissible b
122              The marked neuroprotection from ischemic brain injury in MK2(-/-) mice was not associate
123 , 3 h) produces tolerance 24 h after hypoxic-ischemic brain injury in neonatal rats.
124                                Prevalence of ischemic brain injury in pediatric patients with SCD is
125                                      Hypoxic-ischemic brain injury in premature infants results in ce
126  (IL) 1, and profoundly exacerbated (50-90%) ischemic brain injury in rats and mice, a response that
127 inistered at 24 hrs, but not 48 hrs, worsens ischemic brain injury in rats resuscitated from asphyxia
128                                   Studies of ischemic brain injury in rodents have shown that adminis
129 ntaining preexisting hypertension alleviates ischemic brain injury in SHR by increasing collateral ci
130             We find that the exacerbation of ischemic brain injury in STEP deficient mice involves an
131                                      Hypoxic-ischemic brain injury in survivors of perinatal asphyxia
132 er, high-resolution DWI provides evidence of ischemic brain injury in the majority of TIA patients.
133 d improves neurologic function after hypoxic ischemic brain injury in the newborn piglet.
134                                      Hypoxic-ischemic brain injury in the perinatal period is a major
135 represents an important component of hypoxic-ischemic brain injury in the perinatal period.
136  of a rat CART peptide is protective against ischemic brain injury in vivo.
137 es would cause damage to astrocytes after an ischemic brain injury in vivo.
138 at contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD36
139 s detected in a variety of glial cells after ischemic brain injury, including oligodendrocyte lineage
140 ients on hemodialysis exhibited a pattern of ischemic brain injury (increased fractional anisotropy a
141  due to altered mental status (intoxication, ischemic brain injury), indirect lung injury (non-pulmon
142 ever at onset and in the acute setting after ischemic brain injury, intracerebral hemorrhage, and car
143   Such patients are at high risk for hypoxic-ischemic brain injury, intracranial hemorrhage, cerebral
144                             Neonatal hypoxic-ischemic brain injury is a major cause of neurological d
145                                      Hypoxic/ischemic brain injury is associated with accumulation of
146            While the role of BDNF in hypoxic-ischemic brain injury is not clear, evidence suggests th
147 st that VNS-induced protection against acute ischemic brain injury is not primarily mediated by chang
148                      We also show that acute ischemic brain injury is regulated by mechanisms that re
149 us circulation after cardiac arrest, hypoxic ischemic brain injury is the primary cause of mortality
150    Acute brain injury (ABI) included hypoxic-ischemic brain injury, ischemic stroke, intracranial hem
151                   ABI was defined as hypoxic-ischemic brain injury, ischemic stroke, or intracranial
152 rebral artery occlusion, or neonatal hypoxic-ischemic brain injury, Mn preferentially accumulated in
153 bitors have shown promise in several hypoxic ischemic brain injury models, and we wished to see if th
154                                      Hypoxic-ischemic brain injury occurring in antenatal, perinatal
155                                      Hypoxic-ischemic brain injury occurs frequently in infancy and c
156 nd the etiology of brain death being hypoxic-ischemic brain injury (odds ratio, 2.9; 95% CI, 1.43-5.8
157 ), the etiology of brain death being hypoxic-ischemic brain injury (odds ratio, 3.2; 95% CI, 1.3-8.8;
158 ype mice before subjecting them to a hypoxic-ischemic brain injury or in APP/PS1 mice prior to the fo
159 4.27; 95% CI, 1.71-10.67; P = .002), hypoxic ischemic brain injury (OR, 4.16; 95% CI, 2.13-8.10; P <
160  with improved neurologic outcome in hypoxic ischemic brain injury patients after cardiac arrest.
161 f diffusion limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as de
162                                   In hypoxic-ischemic brain injury patients with brain hypoxia, there
163                          The role of TnC for ischemic brain injury, post-ischemic immune responses an
164 s preliminary study of patients with hypoxic ischemic brain injury postcardiac arrest, goal-directed
165                            Perinatal hypoxic-ischemic brain injury remains a major cause of cerebral
166 chemic stroke, its role in the mechanisms of ischemic brain injury remains controversial.
167  to neuroimaging metrics of brain health and ischemic brain injury, such as normalized whole brain vo
168    Overexpression of human IL-1ra attenuated ischemic brain injury, suggesting that IL-1 may play an
169  with severe anemia to identify unrecognized ischemic brain injury that may have permanent neurocogni
170                            Following hypoxic-ischemic brain injury, the child was taken to the operat
171 nting production of ROSs by NADPH oxidase in ischemic brain injury, the regulatory mechanisms of NADP
172  degrees C) attenuates the release of GLU in ischemic brain injury, this study was designed to detect
173 ssed in the periphery and brain synergize in ischemic brain injury through regulation of the MCP-1/CC
174 flammatory signaling, may also contribute to ischemic brain injury through yet unidentified mechanism
175 studied a rodent model of very early hypoxic-ischemic brain injury to investigate effects of injury o
176 sticity after injury, Rett syndrome, hypoxic-ischemic brain injury, various inborn errors of metaboli
177 t neuron-derived E2 is neuroprotective after ischemic brain injury via a mechanism that involves supp
178 confers long-lasting neuroprotection against ischemic brain injury via a previously unexplored associ
179 ion augments atherosclerosis and exacerbates ischemic brain injury via IL-1 and platelet-mediated sys
180         The salutary effect of DPH-067517 in ischemic brain injury was also observed when the first d
181 he most common involved location for hypoxic-ischemic brain injury was cerebral cortices (82%) and ce
182                                        While ischemic brain injury was more common in venoarterial ex
183                                        Acute ischemic brain injury was seen in 85% of patients with 5
184                                      Hypoxic-ischemic brain injury was the most common type of injury
185 B alterations and inflammation contribute to ischemic brain injury, we examined the role of PGRN in t
186  the Rice-Vannucci model of neonatal hypoxic-ischemic brain injury, we have shown that neuronal degen
187                                      Chronic ischemic brain injuries were studied in 7- and 14-day-ol
188 esponse to cerebral ischemia and its role in ischemic brain injury were investigated.
189 onically hypertensive patient is at risk for ischemic brain injury when perfusion pressure is rapidly
190 rm potentiation of synaptic transmission and ischemic brain injury, whereas ASIC2a is involved in mec
191 treatment in females at risk for cardiac and ischemic brain injury, whereas progesterone appears to b
192  is a multiphasic process involving a direct ischemic brain injury which is then exacerbated by the i
193 in S is a significant neuroprotectant during ischemic brain injury with direct effects on neurons and
194 s an important modulator of the evolution of ischemic brain injury--with hypothermia lessening and hy

 
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