ライフサイエンスコーパス: brain edema

1 the neurovascular unit (NVU) that result in brain edema.

2 by seizures, can initiate symptomatic focal brain edema.

3 n as a novel therapeutic option in vasogenic brain edema.

4 al pressure, cerebral perfusion pressure and brain edema.

5 gittal sinus values concomitant with diffuse brain edema.

6 Mild hypothermia delays ammonia-induced brain edema.

7 on of new therapeutic approaches to treating brain edema.

8 yamines and regional cerebral blood flow and brain edema.

9 ea of incomplete ischemia that is developing brain edema.

10 nal fluid, osmoregulation, and regulation of brain edema.

11 experimental model of vasogenic peritumoral brain edema.

12 his 'glymphatic' system to the main types of brain edema.

13 ing and provide treatment for post-traumatic brain edema.

14 ease of blood-brain barrier permeability and brain edema.

15 tcome in clinical conditions associated with brain edema.

16 ating intracranial hypertension and reducing brain edema.

17 9 (MMP-9) contributes to the pathogenesis of brain edema.

18 reducing inflammatory cell infiltration and brain edema.

19 es, extensive loss of myelinated tracks, and brain edema.

20 owever, RSG reduced neither IgG staining nor brain edema.

21 a similar extent as LPS and also exacerbated brain edema.

22 acterized by cardiac, pulmonary, kidney, and brain edema.

23 in infarct volume (59% to 69%; P:<0.003) and brain edema (50% to 61%; P:<0.05), eliminated brain infi

24 and SR49059 blunted CCI-induced increases in brain edema (79.0+/-0.2%; 9.4+/-0.8microm(2)).

25 The ammonia group exhibited brain edema (79.97 +/- 0.04 vs. 81.11 +/- 0.13% water),

26 Brain edema (80.48 +/- 0.11%) and cerebral hyperemia (14

27 We have shown brain edema, a marked increase in brain glutamine, and a

28 Only the highest dose of fluconazole reduced brain edema after 7 days.

29 sttraumatic brain neutrophil accumulation or brain edema after CCI in rats.

30 neuronal loss in conjunction with attenuated brain edema after cerebral contusion and to reduce brain

31 ere AQP4 deletion protects against cytotoxic brain edema after cerebral ischemia.

32 ge likely predominate in the pathogenesis of brain edema after contusion.

33 inhibition by SR49059 significantly reduced brain edema after cortical contusion injury (CCI) in rat

34 edema after cerebral contusion and to reduce brain edema after focal cerebral ischemia.

35 , TPC) reduces infarct volume and attenuates brain edema after focal cerebral ischemia.

36 ntly reduced neurodeficits and perihematomal brain edema after ICH induction by injection of either a

37 ANC on blood-brain barrier (BBB) damage and brain edema after traumatic brain injury in rats.

38 rmia (33 degrees-35 degreesC) can ameliorate brain edema after traumatic brain injury.

39 evere signs of cerebral malaria with greater brain edema, although disruption of the blood-brain barr

40 This model predictably develops brain edema and a marked increase in CBF at 3 hours of i

41 mmediately after thrombin injections blocked brain edema and BBB disruption.

42 following neurological evaluation to assess brain edema and BBB permeability by IgG staining.

43 Brain edema and cerebral infarct volume were significant

44 NLRP3 knockdown reduced brain edema and decreased myeloperoxidase (MPO) levels a

45 ses vascular permeability, which can lead to brain edema and exacerbate ischemic brain injury.

46 We observed that VPC reduced brain edema and improved neurological function 24 h and

47 duced inflammation, consequently attenuating brain edema and improving of neurological functions afte

48 effective in attenuating short-term effects (brain edema and infarct volume) or long-term effects (br

49 of VEGF reduces ischemia/reperfusion-related brain edema and injury, implicating VEGF in the pathogen

50 Hypothermia reduces brain edema and intracranial pressure in patients with t

51 f a tTG inhibitor, cystamine, on ICH-induced brain edema and neurological deficits.

52 mbolic models of stroke in rats, and reduced brain edema and neuronal loss after traumatic brain inju

53 to investigate 1) the effect of mannitol on brain edema and oxygenation, using a multiparametric mag

54 contrast to the slowed diffusion produced by brain edema and seizure activity, diffusion in the ECS w

55 receiving the 28% polymers developed severe brain edema and seizures, and accrual to this cohort was

56 neuroprotection by furosemide indicate that brain edema and swelling are essential events in the bra

57 ood on hematoma volume, neurologic function, brain edema and swelling, and markers of neuroinflammati

58 Brain edema and the associated increase in intracranial

59 Brain edema and the consequent increase in intracranial

60 2X7R siRNA alleviated neurological deficits, brain edema, and BBB disruption after ICH, in associatio

61 Body weight, neurologic scores, brain edema, and blood-brain barrier disruption were eva

62 llary permeability, progressively escalating brain edema, and damage of the neurovascular unit.

63 suppression prevented neurological deficits, brain edema, and Evans blue extravasation at 24 to 72 ho

64 n decreases neutrophil infiltration, reduces brain edema, and improves neurological function in an in

65 significantly (P<0.05) reduced BBB leakage, brain edema, and ischemic lesion volume compared with ra

66 imals showed blood-brain barrier disruption, brain edema, and neurologic deficits, accompanied with p

67 essed the effects of isosal on hemodynamics, brain edema, and plasma sodium concentration after head

68 ving rapid water transport such as glaucoma, brain edema, and swelling of premature infant lungs.

69 f slow controlled rewarming to avoid rebound brain edema, and the high risk for infectious and cardio

70 In a freeze-injury model of vasogenic brain edema, AQP4-deficient mice had remarkably worse cl

71 Because BBB damage and brain edema are discordant, mechanisms other than BBB da

72 microvascular hyperpermeability followed by brain edema are hallmark features of several brain patho

73 sport and hydrolysis in the mechanism of the brain edema associated with ALF.

74 rized by breakdown of cerebellum and cortex, brain edema, astrocytosis, degeneration of neuronal dend

75 cantly improved neurobehavioral function and brain edema at 24 hrs but not 72 hrs after subarachnoid

76 An ammonia infusion resulted in brain edema at both time points.

77 The 20 patients with brain edema at MR imaging had a significantly greater in

78 Brain edema at MR imaging in patients with preeclampsia-

79 le associations between these parameters and brain edema at MR imaging.

80 analysis showed the PAI-1 treatment reduced brain edema, axonal degeneration, and cortical cell deat

81 SBI causes increased brain edema, BBB disruption and inflammation localized a

82 flammatory changes, however, did not improve brain edema, BBB disruption and neurological outcomes af

83 Outcomes measured included mortality rate, brain edema, BBB disruption, and neurobehavioral testing

84 s in an acute setting, specifically in fatal brain edema (BE) associated with DKA, we studied neurona

85 Brain edema (BE) is an uncommon but life-threatening com

86 patients who died as the result of clinical brain edema(BE)that developed during the treatment of se

87 sion of five-unit thrombin 7 days later with brain edema being assessed after a further 24 h.

88 lt in post-operative complications including brain edema, blood-brain barrier disruption (BBB) and ce

89 treatment group showed significantly reduced brain edema, blood-brain barrier disruption, lesion volu

90 e killed at 4, 8 and 24 h later and used for brain edema, blood-brain barrier permeability, hemorrhag

91 The development of posttraumatic brain edema can limit the oxygen utilization by brain ti

92 r survival than wild-type mice in a model of brain edema caused by acute water intoxication.

93 on was slowed more than sixfold in cytotoxic brain edema caused by anoxia.

94 hours after CSD, plasma protein leakage and brain edema developed contemporaneously.

95 blood-brain barrier (BBB) permeability, yet brain edema does not normally occur during pregnancy.

96 layed cooling for the treatment of cytotoxic brain edema does not provide definitive or lasting treat

97 gated the ability of CD8 T cells to initiate brain edema during ECM.

98 Neurological deficits, brain edema, enzyme-linked immunosorbent assay, Western

99 urological deficits, Fluoro-Jade C staining, brain edema, Evans blue extravasation and fluorescence,

100 ith fulminant hepatic failure (FHF) die with brain edema, exhibiting an increased cerebral blood flow

101 In another model of brain edema, focal ischemic stroke produced by middle ce

102 AQP4-deficient mice showed reduced cellular brain edema following water intoxication and ischemic st

103 factor for the development of infarction by brain edema formation and apoptotic neuronal cell death

104 t of the selective COX-2 inhibitor NS-398 on brain edema formation and cerebral blood flow in a rat m

105 in mouse brain and to evaluate its effect on brain edema formation and infarction after permanent foc

106 animals demonstrate reproducible hematomas, brain edema formation and marked neurological deficits.

107 turation and in brain tissue PO(2) alongside brain edema formation and microvascular lumen collapse a

108 ategy might help to attenuate trauma-induced brain edema formation and neuronal damage as secondary e

109 ctive effects of thrombin preconditioning on brain edema formation are related to this activation.

110 Neither regional brain edema formation at 24 hrs postinjury nor the exten

111 Brain edema formation due to blood-brain barrier (BBB) d

112 Brain edema formation occurs after dysfunctional control

113 ion of a low dose of thrombin attenuates the brain edema formation that results from either an intrac

114 or agonist, biphalin, in decreasing reducing brain edema formation using both in vitro and in vivo mo

115 ermine its effect on secondary brain damage, brain edema formation, and inflammation.

116 arterial blood pressure aggravates regional brain edema formation, regional cell death, and neurolog

117 c function after 24 hrs but failed to reduce brain edema formation.

118 ) is a primary influx route for water during brain edema formation.

119 The role of vasogenic mechanisms of brain edema has not been explored.

120 Three days after intracerebral hemorrhage, brain edema, hematoma volume and the number of apoptotic

121 in injuries, such as brain trauma, localized brain edema, hematoma, focal cerebral ischemia, or brain

122 stidine similarly abolishes OS, the mPT, and brain edema in a rat model of ALF.

123 rovide a new therapeutic option for reducing brain edema in a wide variety of cerebral disorders.

124 molecular mechanism for the pathogenesis of brain edema in acute bacterial meningitis, and suggest t

125 Mechanisms of brain edema in acute liver failure (ALF) are not complet

126 Brain edema in acute liver failure (ALF) remains lethal.

127 a) represents a significant component of the brain edema in ALF, and elevated blood and brain ammonia

128 may thus play an important role in vasogenic brain edema in ALF.

129 role of MMP-9 in the vasogenic mechanism of brain edema in ALF.

130 tion of lipopolysaccharide (LPS) exacerbates brain edema in cirrhotic rats; and if so whether this is

131 TPC also reduced the brain edema in cortex and basal ganglia by 50 and 53% (P

132 "reverse urea effect" in the pathogenesis of brain edema in DDS.DWI may be a useful diagnostic tool f

133 The nature of brain edema in dialysis disequilibrium syndrome (DDS) wa

134 Mild hypothermia prevents brain edema in experimental models and in humans with FH

135 The pathogenesis of brain edema in fulminant hepatic failure is still unreso

136 new insights into hepatic encephalopathy and brain edema in fulminant hepatic failure.

137 Two mechanisms may account for brain edema in fulminant hepatic failure: the osmotic ef

138 e, a commonly used glucocorticoid to prevent brain edema in GBM patients, suppressed the observed inf

139 eramide leads to increased BBB breakdown and brain edema in surgical brain injury.

140 We did not observe astrocyte swelling or brain edema in the acute phase, calling into question cu

141 y (p<0.001), and significantly reduced focal brain edema in the cortex adjacent to the site of maxima

142 r (BBB) disruption due to SBI can exacerbate brain edema in the post-operative period.

143 iation of sodium and potassium with ischemic brain edema in the rodent model, and show that these cla

144 indomethacin will prevent the development of brain edema in this hyperammonemic model.

145 ld hypothermia in a model of ammonia-induced brain edema in which accumulation of brain glutamine has

146 intracerebral hemorrhage (ICH) indicate that brain edema increases progressively in the first 24 h an

147 Our results strongly suggest that the brain edema induced by hemodialysis in uremic rats is du

148 Brain edema is a serious consequence of hemispheric stro

149 Brain edema may occur in infants with galactosemia and h

150 ssment included neurological function tests, brain edema measurement, Evans blue extravasation, immun

151 Our main findings are as follows: brain edema mimicking hypoosmotic conditions stimulates

152 correlated with significant improvements in brain edema, motor coordination, and working memory, and

153 We investigated the role of VEGF165b in brain edema, neutrophil infiltration, ischemic brain dam

154 poorly controlled type 1 diabetes and fatal brain edema of ketoacidosis neuronal deficits associated

155 visceral hypoxic injuries), visualization of brain edema on MR images, and T1 and T2 relaxation times

156 AQP4 deletion in mice reduces cytotoxic brain edema produced by different pathologies.

157 Cytotoxic brain edema (produced by water intoxication) or seizure

158 Brain edema, provoked in part by enhanced cerebrovascula

159 ccount for differences in the development of brain edema seen in acute or chronic liver failure.

160 sults showed that mTBI model did not produce brain edema, skull fracture or sensorimotor coordination

161 igate the role of AQP4 in meningitis-induced brain edema, Streptococcus pneumoniae was injected into

162 ns in neuropathological disorders, including brain edema, stroke, and head injuries.

163 is crucial for fluid clearance in vasogenic brain edema, suggesting AQP4 activation and/or up-regula

164 (thrombin preconditioning; TPC) reduces the brain edema that follows a subsequent intracerebral infu

165 e sought to define the mechanism controlling brain edema through the use of the murine experimental c

166 crease in cerebral perfusion is required for brain edema to become manifest.

167 ffect of recombinant human erythropoietin on brain edema using diffusion-weighted magnetic resonance

168 Brain edema was accompanied by a specific increase in ce

169 Brain edema was detected by calculating water content.

170 Brain edema was estimated at 24 hrs using wet - dry) / w

171 Brain edema was estimated by calculating the edema index

172 razolium chloride (TTC) staining at 24 h and brain edema was measured using the wet/dry weight method

173 n GCSF vs. control; however no difference in brain edema was observed at 24 hrs after injury between

174 Localized brain edema was observed in tissue surrounding the surgi

175 This brain edema was significantly higher in rats subjected t

176 Also, the brain edema was significantly reduced.

177 of alterations of CBF on the development of brain edema, we administered intravenous (IV) indomethac

178 Lesion volume and brain edema were estimated from apparent diffusion coeff

179 Neurobehavioral function and brain edema were evaluated at 24 and 72 hrs.

180 fficulties with wound healing, seizures, and brain edema were noted.

181 Mild intestinal gas distention and brain edema were observed at necropsy in a few mice, whi

182 Greater degrees of hemorrhage and brain edema were observed in collagenase-induced ICH.

183 wmetry and specific gravity, an indicator of brain edema, were measured in contralateral (non-ischemi

184 blue analysis and a trend towards increased brain edema which was significant at 72 h.

185 thioacetamide caused a significant degree of brain edema, which was associated with induction of OS a

186 TPC suppressed thrombin-induced brain edema while PD 098059 blocked this protective effe

187 improved cardiac resuscitability and reduced brain edema, without increasing bleeding complications.

188 ence for enhanced ECS diffusion in vasogenic brain edema, yet greatly slowed diffusion in cytotoxic e