ライフサイエンスコーパス: cerebral edema

1 brain barrier breakdown and life-threatening cerebral edema.

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

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

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

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

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

7 Scanning of the brain showed cerebral edema.

8 such seizure activity to the development of cerebral edema.

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

10 id development of multiple organ failure and cerebral edema.

11 mountaineers who suffered from high-altitude cerebral edema.

12 novel potential approach to the treatment of cerebral edema.

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

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

15 ic brain injury and other diseases involving cerebral edema.

16 No patient died from isolated cerebral edema.

17 e neurovascular unit with the development of cerebral edema.

18 treatment of hemorrhage-induced retinal and cerebral edema.

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

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

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

22 blood flow and the development of vasogenic cerebral edema.

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

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

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

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

27 50 mOsm/L is beneficial for the treatment of cerebral edema; 2) perivascular pool of aquaporin-4 play

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

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

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

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

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

33 Severe pretransplant cerebral edema and a higher posttransplant international

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 Cerebral edema, as measured by percentage of hemispheric

63 Cerebral edema associated with diabetic ketoacidosis is

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Cerebral edema contributes significantly to morbidity an

78 Cerebral edema contributes significantly to morbidity an

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

80 %) experienced bypass-related complications (cerebral edema, femoral vein laceration).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Cerebral edema includes accumulation of extracellular fl

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

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

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

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

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

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

113 Cerebral edema is a key poor prognosticator in traumatic

114 Cerebral edema is a leading cause of mortality in stroke

115 Cerebral edema is a life-threatening complication of dia

116 Cerebral edema is a potentially life-threatening complic

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

118 Cerebral edema is a serious complication of ischemic bra

119 Cerebral edema is a well-recognized and potentially fata

120 Cerebral edema is an uncommon but devastating complicati

121 Cerebral edema is common in severe hepatic encephalopath

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

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

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

125 1/drug vs. 11/vehicle), memory function, and cerebral edema (n=12/drug vs. 13/vehicle).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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