ライフサイエンスコーパス: brain damage

1 both to addictive behaviors and drug-induced brain damage.

2 for prognostic purposes and to assess early brain damage.

3 ous in reducing LPS-induced hypoxic-ischemic brain damage.

4 spreading depression (CSD), which aggravates brain damage.

5 fibrosis and protected against hydrocephalic brain damage.

6 etworks that can be individually impaired by brain damage.

7 ines, leading to the exacerbation of primary brain damage.

8 n modulate attentional impairments following brain damage.

9 orms, NCX1, NCX2, and NCX3, worsens ischemic brain damage.

10 tor molecule-1 (TRIF) did not develop larger brain damage.

11 structural MR imaging markers of subclinical brain damage.

12 tentional impairments in patients with focal brain damage.

13 but also strongly protected against ischemic brain damage.

14 ickly enough with anticonvulsants to prevent brain damage.

15 eizures, or gross or microscopic evidence of brain damage.

16 symptoms; the brain MRIs indicating diffuse brain damage.

17 type W (HERV-W) contributes significantly to brain damage.

18 face recognition deficits in the absence of brain damage.

19 e microRNAs after cardiac arrest may reflect brain damage.

20 function to reduce ischemia-induced hypoxic brain damage.

21 cerebral inflammation and limiting secondary brain damage.

22 we have developed for autoantibody-mediated brain damage.

23 ood flow and significantly reducing ischemic brain damage.

24 f cerebral edema further contributes towards brain damage.

25 since the injury or the extent of structural brain damage.

26 rapeutically targeted to minimize poststroke brain damage.

27 the pathogen from circulation and prevented brain damage.

28 e right-hemisphere following left-hemisphere brain damage.

29 ) was associated with multiple indicators of brain damage.

30 causing swelling of the head and potentially brain damage.

31 st postnatal days and indicators of neonatal brain damage.

32 of motor function in pre-clinical models of brain damage.

33 r derangements that might also contribute to brain damage.

34 maged neurons to form axon collaterals after brain damage.

35 as part of the host inflammatory response to brain damage.

36 terious immune responses and limit bystander brain damage.

37 induce brain Hp is linked to a reduction in brain damage.

38 exacerbates transient focal ischemia-induced brain damage.

39 thus, may result in an increase in ischemic brain damage.

40 and middle cerebral artery occlusion-induced brain damage.

41 r time in children with perinatal unilateral brain damage.

42 sumption on transient focal ischemia-induced brain damage.

43 icular injection of tPA increased HI-induced brain damage.

44 utes to the pathogenesis of hypoxic-ischemic brain damage.

45 ortant functions in many aspects of ischemic brain damage.

46 ism may explain why inhibition of XO reduces brain damage.

47 tective mechanisms that can prevent or limit brain damage.

48 opics ranging from learning to recovery from brain damage.

49 hypoxanthine nor xanthine infusion increased brain damage.

50 w three main roles of astrocytes in ischemic brain damage.

51 strate at the time of injury should increase brain damage.

52 or antagonist abolished the effect of LPS on brain damage.

53 ary acidic protein (GFAP) is associated with brain damage.

54 ediate layers of the SC contralateral to the brain damage.

55 ng destructive molecules that may exacerbate brain damage.

56 cerebral ischemia, significantly aggravates brain damage.

57 induced microvascular thrombus formation and brain damage.

58 al therapeutic target to minimize poststroke brain damage.

59 ce of diffuse vascular and neurodegenerative brain damage.

60 ing in postnatal microcephaly with extensive brain damage.

61 y cells invading the brain lead to secondary brain damage.

62 of high-level visual cortex following focal brain damage.

63 rophages and consequently increases ischemic brain damage.

64 nts the development of clinical symptoms and brain damage.

65 y identify a new therapeutic window to limit brain damage.

66 satory mechanisms used by patients following brain damage.

67 e has been implicated in the pathogenesis of brain damage.

68 verlapping and syndrome-specific patterns of brain damage.

69 rapeutically targeted to minimize poststroke brain damage.

70 modulates poststroke behavioral deficits and brain damage.

71 EST-downstream genes might modulate ischemic brain damage.

72 ding better compensation or resilience after brain damage.

73 infants with MoCD and prevents irreversible brain damage.

74 lly seen in dystonia secondary to structural brain damage.

75 tions can lead to cold sores, blindness, and brain damage.

76 itive function even with a certain amount of brain damages.

77 tality apart from a reduction in the fear of brain damage (-0.0185, CI -0.0313 to -0.0057, p=0.0046)

78 reorganization in somatosensory cortex after brain damage [1] and amputation [2].

79 ted mice had a significantly lower volume of brain damage (13+/-7 mm(3), p<0.01) than both control gr

80 otected from NOX-mediated neuronal death and brain damage 24 h after stroke.

81 In a separate study, brain damage 3 days after stroke was determined histolog

82 rs of injury significantly reduced secondary brain damage (30 mins: 25 mm vs. vehicle: 41 mm) and imp

83 ysfunction, potentially leading to permanent brain damage, a condition known as kernicterus Although

84 , DANGER-deficient mice manifest more severe brain damage after acute excitotoxicity and transient ce

85 s a key role in the development of secondary brain damage after brain trauma.

86 lator that links inflammation and subsequent brain damage after ischaemia.

87 t an L-kynurenine/AhR pathway mediates acute brain damage after stroke and open new possibilities for

88 roinflammation plays a key role in secondary brain damage after stroke.

89 Importantly, examination of patients with brain damage allows one to draw conclusions about whethe

90 NEIL1 deficiency results in increased brain damage and a defective functional outcome in a foc

91 sociation with improved motor function after brain damage and amphetamine treatment linked with rehab

92 These conditions can cause severe brain damage and are a leading cause of death and long-t

93 bial infections, it can also cause permanent brain damage and blindness.

94 tischemic helium at 75 vol% reduces ischemic brain damage and brain hemorrhages.

95 s) during the ischemic period and aggravates brain damage and cell death after ischemic injury.

96 this issue, the current study examined frank brain damage and changes in cortical activation as predi

97 tigation against severe hypoglycemia-induced brain damage and cognitive dysfunction.

98 onsible for the accumulation of irreversible brain damage and for the development of innovative thera

99 Brain damage and functional impairment were reduced by I

100 but they encompass a spectrum of severity of brain damage and have indistinct boundaries.

101 Administration of Ex-4 reduced brain damage and improved functional outcome in a transi

102 candesartan afforded sustained reduction of brain damage and improved neurologic function 5 days aft

103 ptic density-95 (PSD-95) can reduce ischemic brain damage and inflammatory pain in rodents.

104 h often runs in families, have no history of brain damage and intact early visual processing systems.

105 ve STEP during reperfusion precedes ischemic brain damage and is associated with secondary activation

106 Brain damage and ischemia often trigger cortical spreadi

107 Status epilepticus (SE) can cause brain damage and lead to neural dysfunction.

108 ient female mice showed a marked increase in brain damage and long-lasting learning deficits, whereas

109 ity into the brain, microvascular structural brain damage and lower scores in various cognitive domai

110 ical conditions result from diverse areas of brain damage and may have different underlying causes.

111 zzle of the relationship between PrP(Sc) and brain damage and may in part explain the mechanism of pr

112 the effect of neonatal hypoxic-ischemic (HI) brain damage and mesenchymal stem cell (MSC) treatment o

113 nduce intracerebral hemorrhage caused marked brain damage and modified the levels of inflammatory mar

114 tudied whether alpha-Syn mediates poststroke brain damage and more importantly whether preventing alp

115 Brain damage and neurological deficit 24 h after MCAo we

116 chemia/reperfusion injury, and the amount of brain damage and neurological deficits caused by a strok

117 ce are profoundly protected from excitotoxic brain damage and neurological deficits following experim

118 f and how these factors affect the extent of brain damage and outcome in ischemic stroke.

119 these mice to experience significantly more brain damage and oxidative stress in response to middle

120 ine model of atherosclerosis showed vascular brain damage and peripheral inflammation.

121 romised during aging, resulting in increased brain damage and poorer functional outcome.

122 V isolate (MR-766) is more potent at causing brain damage and postnatal lethality than MEX1-44.

123 ompared with controls, due to a reduction in brain damage and reduced accumulation of amyloid beta ag

124 Severe hypoglycemia induced brain damage and striking deficits in spatial learning a

125 s with acquired cognitive deficits following brain damage and studies using contemporary neuroimaging

126 drial iron in the pathogenesis of SE-induced brain damage and subcellular iron chelation as a novel t

127 l hypoxia-ischemia (HI) is a common cause of brain damage and subsequent behavioral deficits in prema

128 iomarkers in sera of ill children reflecting brain damage and T. gondii infection.

129 n significantly interfere with recovery from brain damage and that mitigation of maladaptive effects

130 bolysis and subsequent reduction of ischemic brain damage and that postischemic helium at 75 vol% red

131 potential to identify specific mechanisms of brain damage and to better target treatment to individua

132 Treatment aims to prevent additional brain damage and to optimise conditions for brain recove

133 ical symptoms to neuroanatomical profiles of brain damage and ultimately to tissue pathology is a key

134 serious consequences in neonates, provoking brain damage and/or sudden death due to apnea episodes a

135 Whereas both brain-damaged and healthy controls used comparisons betw

136 born very preterm have an increased risk of brain damage, and brain abnormalities which persist into

137 1A1 activity that can lead to CNS toxicity, brain damage, and even death.

138 e calculated in and around the site of focal brain damage, and in selected distant and subcortical br

139 these syndromes with the syndromes of acute brain damage, and indicate how the clinical syndromes re

140 ain edema, neutrophil infiltration, ischemic brain damage, and neuronal death in vivo using an adenov

141 Ischemia is a major cause of brain damage, and patient management is complicated by t

142 ed, hyperglycemia did not aggravate ischemic brain damage any longer.

143 egulation defects following focal prefrontal brain damage are associated with exceptionally irrationa

144 eral homonymous visual field disorders after brain damage are frequently associated with a severe imp

145 pression, and recovery of function following brain damage are mediated, in part, by the release of br

146 o are fully conscious and awake, yet, due to brain damage, are unable to show any behavioral responsi

147 PC significantly reduced brain damage as measured by weight loss of the right hem

148 e previously observed TBI severity-dependent brain damage as revealed by 2,3,5-triphenyltetrazolium c

149 received mild induced hypothermia to reduce brain damage as suggested by cardiopulmonary resuscitati

150 l effects of aortic stiffening may result in brain damage as well as heart failure.

151 s with neonatal hypoxic-ischemic and gliotic brain damage, as well as in active multiple sclerosis le

152 is responsible for a substantial fraction of brain damage at early time points after ischemic stroke

153 This process and the associated brain damage begin years before the substantial neurodeg

154 trauma to determine its effect on secondary brain damage, brain edema formation, and inflammation.

155 Brain damage, brain water content, and behavioral assess

156 onounced inflammatory response that mediates brain damage but is also essential for the tissue repara

157 ch can defend the brain against hypoglycemic brain damage but may aggravate brain damage during ische

158 stroke not only produces local ischemia and brain damage, but also has profound effects on periphera

159 s a potential strategy for treating ischemic brain damage, but high-affinity inhibitors are lacking.

160 or (TNF) is significantly upregulated during brain damage, but it is unknown whether TNF influences s

161 d T cells as important mediators of ischemic brain damage, but the contribution of the different T-ce

162 he observation that inhibition of XO reduces brain damage, but the precise mechanism by which the enz

163 ts down-regulation is a promoter of ischemic brain damage by acting through its target DNMT3a.

164 has been proposed to contribute to secondary brain damage by causing pericontusional ischemia, but pr

165 ice are responsible for reducing H/I-induced brain damage by decreasing extracellular glutamate accum

166 al neurotoxicity from salvage treatments and brain damage by relapsing tumor.

167 at laropiprant treatment post-ICH attenuates brain damage by targeting primary as well as secondary i

168 In the brain damaged by injuries or neurological diseases, spin

169 Unilateral brain damage can lead to a striking deficit in awareness

170 tic or anti-TNF antibody treatment prevented brain damage caused by E. coli.

171 RBC/tPA neither aggravated brain damage caused by focal ischemia in a filament mode

172 or performance in rats subjected to ischemic brain damage caused by permanent middle cerebral artery

173 leeds are hypothesized downstream markers of brain damage caused by vascular and amyloid pathologic m

174 Brain damage causing acquired amusia disrupts the functi

175 Fear of brain damage, coma, convulsions, death and dehydration w

176 d the topological distribution of structural brain damage, defined as post-stroke necrosis or cortica

177 The pathophysiological mechanisms of brain damage depend on brain maturation at the time of s

178 gy with an extended time window for reducing brain damage due to stroke by activating particular PKC

179 Brain damage due to stroke or traumatic brain injury (TB

180 Increased ischemic brain damage during alcohol consumption may be related t

181 mpus and a possible target molecule to limit brain damage during hemorrhagic stroke.

182 hypoglycemic brain damage but may aggravate brain damage during ischemia due to enhanced lactic acid

183 uding Alzheimer's disease, ALS, and ischemic brain damage (elevated d-serine) and schizophrenia (redu

184 l models to link infection, inflammation and brain damage exist, but proof of causation is elusive.

185 to alcohol prenatally may suffer from severe brain damage, expressed as a variety of behavioral probl

186 atients with cerebrovascular accidents where brain damage extends into subcortical white matter.

187 monstrated their limited capacity to prevent brain damage following ischemia.

188 sults were robust to the effects of possible brain damage from suicide attempts, depressive severity,

189 se transmitters with known roles in ischemic brain damage: glutamate, D-serine, ATP and adenosine.

190 Lack of objective biomarkers for brain damage hampers acute diagnosis and clinical decisi

191 Previous research on recovery from brain damage has focused primarily on adaptive plasticit

192 developing rat brains with hypoxic-ischemic brain damage (HIBD).

193 ds promise for understanding situations when brain damage impairs normal function or failure to regul

194 the brain, hyperglycemia aggravates ischemic brain damage in acute stroke.

195 totic and anti-excitotoxic actions, reducing brain damage in adult animal models of brain injury.

196 tive antibiotic treatment and contributes to brain damage in bacterial meningitis.

197 after global cerebral ischemia (GCI)-induced brain damage in C57black6 mice.

198 public health concern because of its link to brain damage in developing human fetuses.

199 on differences in the location and extent of brain damage in different patient groups.

200 Seizure-driven brain damage in epilepsy accumulates over time, especial

201 te to the overall burden of vascular-related brain damage in intracerebral haemorrhage, and may be a

202 and invasiveness in cancer cells and worsens brain damage in ischemic stroke.

203 ic strategies with the potential to minimize brain damage in ischemic stroke.

204 hic effects cannot explain the phenotypes of brain damage in most infected infants.

205 echniques, we aimed to characterize vascular brain damage in old ApoE(-/-) mice fed a high-cholestero

206 able neuroprotective strategy for minimizing brain damage in premature infants with intraventricular

207 expression of miR-96 significantly prevented brain damage in SE rats by inhibiting Atg7 and Atg16L1 e

208 38 MAPK activation but also reduces ischemic brain damage in STEP KO mice.

209 dingly, we investigated whether NOX-mediated brain damage in stroke can be inhibited by suppression o

210 on of glutamatergic receptors contributes to brain damage in stroke.

211 ia differs from other, more complex types of brain damage in that it appears not to recruit activin A

212 F) biomarkers for AD suggest the presence of brain damage in the preclinical stage of AD.

213 Specifically, patients whose brain damage included regions commonly associated with l

214 specific emotional deficits following focal brain damage (including fear and the amygdala), and the

215 i) mice exhibit manifestations of kidney and brain damage, including increased plasma urea, impaired

216 level and MR imaging markers of subclinical brain damage, including volumetric, focal, and microstru

217 administration of NR but not NAD(+) reduces brain damage induced by NMDA injection.

218 ese responses may be primarily a reaction to brain damage induced by prion infection rather than spec

219 ion, decorin protected against hydrocephalic brain damage inferred from attenuation of glial and infl

220 urrently available to limit the catastrophic brain damage initiated by the development of intraventri

221 Motor learning and functional recovery from brain damage involve changes in the strength of synaptic

222 We found that smokers with brain damage involving the insula, a region implicated i

223 Highly localized vascular brain damage is a frequent finding in this ageing athero

224 Prevention of these apoptotic waves of brain damage is a realistic goal in view of the long del

225 tation of dementia, significant irreversible brain damage is already present, rendering the diagnosis

226 demonstrate that the microglial response to brain damage is also TAM-regulated, as TAM-deficient mic

227 to guide the identification of regions where brain damage is likely to cause persistent behavioural e

228 Seizure-induced brain damage is not conclusively demonstrated either in

229 difficult to demonstrate in humans, because brain damage is rarely restricted to this structure.

230 Poor memory after brain damage is usually considered to be a result of inf

231 g and understanding rehabilitation following brain damage is whether recovery involves new and aberra

232 l skilled behaviors and, when impaired after brain damage, it generates significant disability.

233 jaundice, which can further cause permanent brain damage, kernicterus.

234 al conditions, including cancer and ischemic brain damage, makes Hv1 a promising drug target.

235 ent seizures do not induce the expression of brain damage markers in nonlesional epileptogenic cortex

236 s have recently been raised that subclinical brain damage may occur because of microembolization duri

237 e derangements associated with indicators of brain damage might be indicators of immaturity/vulnerabi

238 genetically aggravates the ischemia-induced brain damage, motor deficits and mortality.

239 ment in spatial navigation in the absence of brain damage, neurological conditions, or basic perceptu

240 us urges, were more likely than smokers with brain damage not involving the insula to undergo a disru

241 d a lower risk of the composite end point of brain damage, nursing home admission, or death (hazard r

242 re relevant to consider treatments to reduce brain damage occurring with transient ischaemic attacks.

243 linicians to answer the question whether the brain damage of the newborn is responsible for its clini

244 patients with semantic impairments following brain damage offer key insights into the cognitive and n

245 viduals with DTD have no apparent structural brain damage on conventional imaging and the neural mech

246 vital importance for assessing the impact of brain damage on function and also for designing rehabili

247 l as for assessing the effects of unilateral brain damage on function.

248 of heart disease, and markers of subclinical brain damage on magnetic resonance (MR) images in commun

249 in the setting of hypoglycemia, resulting in brain damage or death if untreated.

250 ral integrity in the left-hemisphere through brain damage or healthy ageing results in increased righ

251 defibrillation were associated with risks of brain damage or nursing home admission and of death from

252 data and reported the 1-year risks of anoxic brain damage or nursing home admission and of death from

253 ed from 2.1% to 16.8% (P<0.001), the rate of brain damage or nursing home admission decreased from 10

254 bystander CPR was associated with a risk of brain damage or nursing home admission that was signific

255 ry cytokine that is induced in astrocytes by brain damage or seizure.

256 from 2001 through 2012, a total of 10.5% had brain damage or were admitted to a nursing home and 9.7%

257 cannabis in heavy use can cause irreversible brain damage, particularly to adolescents, and thus whet

258 The cognitive impairments shown by brain-damaged patients emphasize the role of task diffic

259 Chronic visual neglect prevents brain-damaged patients from returning to an independent

260 nd cognition critically depends on data from brain-damaged patients since these provide major constra

261 Studies of brain-damaged patients suggest that knowledge of nouns a

262 erent control groups, one of which comprised brain-damaged patients with spared ventral cortex (n > 5

263 y and the level of consciousness in severely brain-damaged patients.

264 l (auditory, visual) integration tasks to 16 brain-damaged patients.

265 perfusion therapies, and help prevent subtle brain damage potentially contributing to long-term cogni

266 We relate localized mechanical brain damage predicted from biofidelic finite element si

267 The immune system participates in the brain damage produced by ischemia, and the damaged brain

268 injury, we examined the role of PGRN in the brain damage produced by ischemia-reperfusion.

269 ink between insomnia and a discrete locus of brain damage, providing novel insight into the neurobiol

270 dation, but mechanisms of alcohol-associated brain damage remain elusive.

271 ental mechanisms underlying alcohol-mediated brain damage remain unclear.

272 poxia-ischemia (H-I) is the leading cause of brain damage resulting from birth complications.

273 Brain damage resulting in loss of sensory stimulation ca

274 ith the nonparetic limb following unilateral brain damage results in aberrant synaptogenesis, potenti

275 idual blood gas derangements do not increase brain damage risk.

276 eurorehabilitation of anomic patients, whose brain damage spares this region.

277 However, compensation following brain damage suggests that these circuits are capable of

278 ral, and motor symptoms linked to cumulative brain damage sustained from single, episodic, or repetit

279 lineage is more toxic and causes more potent brain damage than the Asian lineage.

280 sponses, are responsible for surveillance of brain damage that frequently results in seizures.

281 n-fluent aphasia, the current study examined brain damage that negatively influences speech fluency i

282 utions of both Zn(2+) and Ca(2+) in ischemic brain damage, the relative importance of each cation to

283 Given the recognized role of INa in hypoxic brain damage, the SUMO pathway and NaV1.2 are identified

284 sient insults to brain may lead to long-term brain damage, these findings suggest that isoflurane may

285 al ischemia and reperfusion is implicated in brain damage through different cellular and molecular me

286 n-symptom mapping in 241 patients with focal brain damage to investigate their neural underpinnings.

287 In addition to immediate brain damage, traumatic brain injury (TBI) initiates a c

288 xecutive function in 182 patients with focal brain damage using voxel-based lesion-symptom mapping.

289 l substrates of g in 241 patients with focal brain damage using voxel-based lesion-symptom mapping.

290 Excessive Zn(2+) causes brain damage via promoting ROS generation.

291 flammation outcomes were assessed at 72 hrs; brain damage was assessed at 2 wks and 6 wks along with

292 Brain damage was confirmed through intrauterine ultrason

293 significance of severe hypoglycemia-induced brain damage was evaluated by motor and cognitive testin

294 Ischemic brain damage was measured by determining stroke volume a

295 h P301L mutation also affects stroke-induced brain damage, we performed hypoxia/ischemia (H/I) in you

296 ia-reoxygenation injury and reduces ischemic brain damage when injected up to 6 h after the insult.

297 sive neuronal death and BBB leakage indicate brain damage, which is further supported by extensive mi

298 d hypohaptoglobinemia aggravates ICH-induced brain damage while pharmacologic intervention with sulfo

299 ain parenchyma, and they respond promptly to brain damage with targeted process movement toward the i

300 minutes after complete occlusion and reduced brain damage without inducing hemorrhage, whereas tirofi