ライフサイエンスコーパス: cerebral edema

1 s known to increase immune cell invasion and cerebral edema.

2 mannitol on total lung water, as well as on cerebral edema.

3 brain barrier breakdown and life-threatening cerebral edema.

4 cle was used as a radiographic surrogate for cerebral edema.

5 d with bicarbonate are at increased risk for cerebral edema.

6 s result from hyperthermia, hyponatremia, or cerebral edema.

7 ars to be a promising therapy for control of cerebral edema.

8 Scanning of the brain showed cerebral edema.

9 such seizure activity to the development of cerebral edema.

10 ic brain injury and other diseases involving cerebral edema.

11 ents had hypoxemia (PO2 = 63 [25] mm Hg) and cerebral edema.

12 id development of multiple organ failure and cerebral edema.

13 for life-threatening mass effect (LTME) from cerebral edema.

14 d to severe encephalopathy, seizures, and/or cerebral edema.

15 ated through reduction in infarct growth and cerebral edema.

16 al of this initial bolus is to quickly treat cerebral edema.

17 mountaineers who suffered from high-altitude cerebral edema.

18 obtundation, and in some cases seizures and cerebral edema.

19 novel potential approach to the treatment of cerebral edema.

20 vidence of cerebral edema, and 11 had severe cerebral edema.

21 -altitude pulmonary edema, and high-altitude cerebral edema.

22 No patient died from isolated cerebral edema.

23 agenlecleucel, cytokine release syndrome, or cerebral edema.

24 e neurovascular unit with the development of cerebral edema.

25 treatment of hemorrhage-induced retinal and cerebral edema.

26 d in a mildly hyperosmotic state to minimize cerebral edema.

27 ure in patients with acute liver failure and cerebral edema.

28 d mannitol as an effective means of reducing cerebral edema.

29 blood flow and the development of vasogenic cerebral edema.

30 ts had changes in brain volume without overt cerebral edema.

31 stroke and trauma, are often exacerbated by cerebral edema.

32 50 mOsm/L is beneficial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 play

33 lepticus (5.7%), motor deficits (12.4%), and cerebral edema (7.9%) were more prevalent.

34 We conclude that cerebral edema, a previously unrecognized complication,

35 Understanding how the timing of cerebral edema affects risk of unfavorable discharge has

36 Neurologic deteriorations related to cerebral edema after massive middle cerebral artery infa

37 Similar to the experience in patients with cerebral edema after other neurologic insults, hypotherm

38 nt effectiveness to progesterone in reducing cerebral edema after TBI.

39 eatment with bicarbonate was associated with cerebral edema, after adjustment for other covariates (r

40 Severe pretransplant cerebral edema and a higher posttransplant international

41 stemic and neuroinflammation as the cause of cerebral edema and blood-brain barrier (BBB) dysfunction

42 were significantly associated with improved cerebral edema and clinical outcome.

43 evere, fluid imbalance can lead to seizures, cerebral edema and death.

44 e blood-brain barrier injury with subsequent cerebral edema and devastating brain hemorrhage.

45 date reporting on the use of HS in treating cerebral edema and elevated ICP include case reports, ca

46 he treatment of patients with post-traumatic cerebral edema and elevated intracranial pressure result

47 A clinical diagnosis of cerebral edema and increased intracranial pressure was m

48 eport that the deleterious effects of tPA on cerebral edema and intracranial bleeding are separable f

49 ther neurologic insults, hypothermia reduces cerebral edema and intracranial hypertension in patients

50 ffecting cerebral blood flow and the risk of cerebral edema and ischemia after acute brain injury.

51 uids restore cerebral perfusion with reduced cerebral edema and modulate inflammatory response to red

52 The pathophysiologic basis of cerebral edema and molecular mechanisms of edema underly

53 e large vessel occlusion was associated with cerebral edema and poor clinical outcomes in patients wh

54 icantly associated with severe pretransplant cerebral edema and postoperative international normalize

55 dels and has been used to treat perilesional cerebral edema and radiation necrosis.

56 wn of the blood-brain barrier (BBB) leads to cerebral edema and reduced blood flow.

57 have clinical implications for patients with cerebral edema and related disorders.

58 to the intracellular compartment can lead to cerebral edema and serious neurological complications, e

59 mm(3) vs. 177.06 +/- 13.21 mm(3)), prevented cerebral edema and significantly improved all neurologic

60 potentially fatal condition associated with cerebral edema and the breakdown of the blood-brain barr

61 Knockout of sST2 reduced post-stroke cerebral edema and was associated with increased stainin

62 re activity, 32 had radiological evidence of cerebral edema, and 11 had severe cerebral edema.

63 hage, loss of consciousness at ictus, global cerebral edema, and a composite score of physiological d

64 d a reduced rate of neurologic decline, less cerebral edema, and a decrease in microglia activation i

65 hemic brain injury, intracranial hemorrhage, cerebral edema, and brain death.

66 ood flow and oxygen extraction by the brain, cerebral edema, and disruption of the blood-brain barrie

67 ed brain infarct volume, neuronal apoptosis, cerebral edema, and improved neurological scores.

68 of neurological damage, effectively relieves cerebral edema, and improves cognitive function in SAH m

69 t significantly improved the mortality rate, cerebral edema, and neurobehavioral deficits; apoptotic

70 e child in the standard-dose group developed cerebral edema, and no deaths occurred during the study

71 Complications such as death, renal failure, cerebral edema, and shock were more prevalent during the

72 nnel is crucially involved in development of cerebral edema, and that targeting SUR1 may provide a ne

73 Although the prevalence of cerebral edema appears to be decreasing, patients with r

74 Intracranial hypertension and cerebral edema are known contributors to secondary brain

75 Pharmacoresistant seizures and cytotoxic cerebral edema are serious complications of ischemic and

76 Brain tumor-associated cerebral edema arises because tumor capillaries lack nor

77 E-deficient animals had a greater degree of cerebral edema as compared to matched controls.

78 Cerebral edema, as measured by percentage of hemispheric

79 Cerebral edema associated with diabetic ketoacidosis is

80 treatment with hypertonic saline attenuates cerebral edema associated with experimental ischemic str

81 motherapy with hypertonic saline ameliorates cerebral edema associated with experimental ischemic str

82 as the clinical manifestation of a low-grade cerebral edema associated with oxidative-nitrosative str

83 isplay severe neurotoxicity, including fatal cerebral edema associated with T cell infiltration into

84 age 65.9 vs 61.7, P = .004) and findings of cerebral edema at index hospitalization (aOR 2.16, P < .

85 Accordingly, cerebral edema attributable to ischemic stroke-induced v

86 kg, and there were no deaths or instances of cerebral edema attributable to product toxicity.

87 s reflects the benefits of FPSA treatment on cerebral edema before ICP.

88 ine are promising experimental approaches to cerebral edema but emergency liver transplantation is th

89 luggish CBF compared to CMS patients without cerebral edema; but what triggers this complication is u

90 rkhead transcription factor, Foxo3a, induces cerebral edema by increasing the AQP4 level in the contr

91 altitude, stroke, or traumatic brain injury, cerebral edema can develop.

92 Cerebral edema (CE) is a potentially life-threatening co

93 gs, but case reports regarding hyperthermia, cerebral edema, cerebral vasospasm, and lethal interacti

94 evelop hyperammonemia, which can progress to cerebral edema, coma, and death, outcomes ameliorated by

95 Its importance in fluid regulation in cerebral edema conditions has been highlighted in severa

96 Autopsy evaluation of sibling 1 revealed cerebral edema consistent with hypoxic ischemic encepath

97 Cerebral edema contributes significantly to morbidity an

98 Cerebral edema contributes significantly to morbidity an

99 ose commercial development was halted due to cerebral edema deaths during a separate pharma-sponsored

100 Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical

101 %) experienced bypass-related complications (cerebral edema, femoral vein laceration).

102 c drainage of CSF would promote clearance of cerebral edema fluid during infection with the neurotrop

103 atures suggestive of cytotoxic and vasogenic cerebral edema followed by microhemorrhages in 2 adult U

104 smotherapy with hypertonic saline attenuates cerebral edema following experimental cardiac arrest and

105 is an important factor in the development of cerebral edema following stroke and any changes in its f

106 of arterial carbon dioxide (relative risk of cerebral edema for each decrease of 7.8 mm Hg [represent

107 ea nitrogen concentrations (relative risk of cerebral edema for each increase of 9 mg per deciliter [

108 d reduced infarct size, necrotic injury, and cerebral edema formation after middle cerebral artery oc

109 motor function, spatial memory deficits, and cerebral edema formation following lateral (parasagittal

110 Dopexamine protects against cerebral edema formation in sepsis by stimulation of bet

111 Cerebral edema frequently develops in the setting of bra

112 e of cerebral ischemia, where development of cerebral edema further contributes towards brain damage.

113 ren and 174 children matched to those in the cerebral-edema group with respect to age at presentation

114 A comparison of the children in the cerebral-edema group with those in the random control gr

115 generally remote environments, high-altitude cerebral edema (HACE) has received little scientific att

116 acidosis within a 15-year period and in whom cerebral edema had developed.

117 Patients with high-altitude cerebral edema have similar splenial-predominant magneti

118 anial hypertension is though to be caused by cerebral edema, high cerebrospinal fluid outflow resista

119 monary edema in 22 (1.7%), and high-altitude cerebral edema in 13 (0.98%) patients.

120 erammonemia is a key contributing factor for cerebral edema in acute liver failure.

121 findings suggest that the pathophysiology of cerebral edema in diabetic ketoacidosis may involve a tr

122 erebral perfusion pressure and a decrease in cerebral edema in hypothermic meningitic animals.

123 c symptoms to life-threatening high-altitude cerebral edema in less than 1% of patients.

124 ons available in 19 patients showed signs of cerebral edema in only 2 (22%) of the phenytoin-treated

125 oncontrast head CT enables quantification of cerebral edema in patients with acute ischemic stroke (A

126 We sought to determine whether cerebral edema in patients with diabetic ketoacidosis wa

127 fusion appears to be a promising therapy for cerebral edema in patients with head trauma or postopera

128 icates that MMP-9 may contribute to observed cerebral edema in peripheral thermal injury.

129 hesis that bolus hypertonic saline decreases cerebral edema in severe hepatic encephalopathy utilizin

130 ay be useful quantitative measures to assess cerebral edema in severe hepatic encephalopathy.

131 Here, we found that ICBs induce cerebral edema in some patients and mice with glioblasto

132 The mechanism of hepatic encephalopathy and cerebral edema in this setting continues to be elucidate

133 Cerebral edema includes accumulation of extracellular fl

134 of SUR1 with low-dose glibenclamide reduced cerebral edema, infarct volume and mortality by 50%, wit

135 een shown to be highly effective in reducing cerebral edema, infarct volume and mortality in adult ra

136 otic homeostasis resulting in cell swelling (cerebral edema), inflammation, and apoptosis.

137 cutely administered, can dramatically reduce cerebral edema, inflammation, tissue necrosis, and progr

138 In severe cases of cerebral edema, intracranial hypertension develops and l

139 onses are associated with the development of cerebral edema, intracranial hypertension, and secondary

140 Space occupying cerebral edema is a feared complication after large isch

141 Cerebral edema is a key poor prognosticator in traumatic

142 Cerebral edema is a leading cause of mortality in stroke

143 Cerebral edema is a life-threatening complication of dia

144 Cerebral edema is a potentially life-threatening complic

145 Isolated experiments suggest that global cerebral edema is a sequela of large hemispheric ischemi

146 Cerebral edema is a serious complication of ischemic bra

147 Cerebral edema is a well-recognized and potentially fata

148 Cerebral edema is an uncommon but devastating complicati

149 Cerebral edema is common in severe hepatic encephalopath

150 If severe pretransplant cerebral edema is confirmed, efforts should be made to a

151 arthria, congenital ataxia and, in one case, cerebral edema leading ultimately to death.

152 pitalization, an intracranial hemorrhage and cerebral edema led to an abrupt deterioration in his neu

153 f an acute neuroinflammatory process, and/or cerebral edema may predict better functional outcome.

154 ase in MT expression preceded an increase in cerebral edema measured with T2-weighted magnetic resona

155 sis framework to quantify infarct growth and cerebral edema (midline shift) mediation effect on succe

156 vere encephalopathy (n = 5), acute fulminant cerebral edema (n = 2), and Guillain-Barre syndrome (n =

157 ndrome/variants (n = 4), and acute fulminant cerebral edema (n = 4).

158 1/drug vs. 11/vehicle), memory function, and cerebral edema (n=12/drug vs. 13/vehicle).

159 is critical to recognize the early signs of cerebral edema (nausea, vomiting, and headache) and inte

160 sions in foetuses like haemorrhages, diffuse cerebral edema, necrotizing encephalitis and decreased b

161 es not appear to affect cerebral infarction, cerebral edema nor the mitochondrial signaling pathway f

162 Cerebral edema occurs in up to 80% of patients with Grad

163 led showing >=25% reduction in the volume of cerebral edema on fluid-attenuated inversion recovery-ma

164 Malignant EEG patterns and global cerebral edema on head computed tomography (CT) were ass

165 th neurological deterioration showed diffuse cerebral edema on imaging and more deranged cerebral hem

166 ent < or =8, pediatric trauma score < or =8, cerebral edema or diffuse axonal injury on initial head

167 Amyloid-related cerebral edema or effusions (mostly asymptomatic) occurr

168 unclear whether brain swelling is caused by cerebral edema or vascular congestion-two pathological c

169 e (OR, 15.38; 95% CI, 2.41-98.18; P = .004), cerebral edema (OR, 8.49; 95% CI, 5.57-12.93; P < .001),

170 ications of severe electrolyte disturbances, cerebral edema, or uncontrolled hemorrhage are uncommon

171 Brain injury induced significant cerebral edema (p < .001) in vulnerable brain regions an

172 aphic scan, and a higher frequency of global cerebral edema (P < .001).

173 bove the autoregulatory limit) may result in cerebral edema, persistent vasodilation, and brain injur

174 These data demonstrate that cerebral edema persists in both injured and contralatera

175 sis in children is associated with vasogenic cerebral edema, possibly due to the release of destructi

176 emia-induced CCC phosphorylation, attenuates cerebral edema, protects against brain damage, and impro

177 and treating patients with life-threatening cerebral edema remain critically important but difficult

178 Pulmonary and cerebral edema resolved as the sodium level increased.

179 Microvascular hyperpermeability and cerebral edema resulting from BBB dysfunction after TBI

180 ers, pulmonary edema, traumatic lung injury, cerebral edema resulting from stroke, and others), it is

181 ntations, such as CAR T-cell therapy-related cerebral edema, severe motor complications or late-onset

182 piratory distress syndrome and high-altitude cerebral edema show congruent cerebral injuries.

183 Upon reperfusion, cerebral edema slowly developed and peaked at 24 hr as s

184 similarity of this syndrome to high-altitude cerebral edema suggests a possible common pathophysiolog

185 h nonparasagittal tumors developed worsening cerebral edema that necessitated the administration of s

186 Thrombin mediates the life-threatening cerebral edema that occurs after intracerebral hemorrhag

187 e of ionic extracellular edema, a subtype of cerebral edema that was only recently specified as an in

188 Two patients had grade-4 adverse events (cerebral edema) that were deemed at least possibly treat

189 er enzymes, and low platelets) syndrome, and cerebral edema-the clinical signs of preeclampsia and ec

190 sis symptoms before and after treatment, the cerebral edema volume, the cerebral necrosis volume, and

191 n the matched control group also showed that cerebral edema was associated with lower partial pressur

192 Subcortical white matter cytoxic cerebral edema was common in severe cases.

193 Maximal cerebral edema was measured at 2 days in both hemisphere

194 No difference in cerebral edema was observed between mice that received V

195 hose in the random control group showed that cerebral edema was significantly associated with lower i

196 ldren with diabetic ketoacidosis but without cerebral edema were also identified: 181 randomly select

197 ped fulminant hepatic failure complicated by cerebral edema, were taking LipoKinetix alone at the tim

198 th 13l resulted in a significant decrease in cerebral edema when administered postinjury.

199 urological critical care is the treatment of cerebral edema, when possible, and the control of life-t

200 A comparison of the children with cerebral edema with those in the matched control group a