ライフサイエンスコーパス: brain damage

1 rophages and consequently increases ischemic brain damage.

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

3 satory mechanisms used by patients following brain damage.

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

5 verlapping and syndrome-specific patterns of brain damage.

6 rapeutically targeted to minimize poststroke brain damage.

7 modulates poststroke behavioral deficits and brain damage.

8 EST-downstream genes might modulate ischemic brain damage.

9 ding better compensation or resilience after brain damage.

10 lly seen in dystonia secondary to structural brain damage.

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

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

13 for prognostic purposes and to assess early brain damage.

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

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

16 fibrosis and protected against hydrocephalic brain damage.

17 to deviate, potentially explained by earlier brain damage.

18 etworks that can be individually impaired by brain damage.

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

20 n modulate attentional impairments following brain damage.

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

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

23 tentional impairments in patients with focal brain damage.

24 but also strongly protected against ischemic brain damage.

25 ickly enough with anticonvulsants to prevent brain damage.

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

27 consistent predictors of clinically relevant brain damage.

28 symptoms; the brain MRIs indicating diffuse brain damage.

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

30 face recognition deficits in the absence of brain damage.

31 e microRNAs after cardiac arrest may reflect brain damage.

32 function to reduce ischemia-induced hypoxic brain damage.

33 gy are two key elements involved in ischemic brain damage.

34 cerebral inflammation and limiting secondary brain damage.

35 we have developed for autoantibody-mediated brain damage.

36 ood flow and significantly reducing ischemic brain damage.

37 f cerebral edema further contributes towards brain damage.

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

39 the pathogen from circulation and prevented brain damage.

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

41 ) was associated with multiple indicators of brain damage.

42 st postnatal days and indicators of neonatal brain damage.

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

44 r derangements that might also contribute to brain damage.

45 maged neurons to form axon collaterals after brain damage.

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

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

48 exacerbates transient focal ischemia-induced brain damage.

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

50 r time in children with perinatal unilateral brain damage.

51 sumption on transient focal ischemia-induced brain damage.

52 glutamate transporter, GLT-1 after ischemic brain damage.

53 So far, drugs are not available to repair brain damage.

54 odel showed improved behavior and alleviated brain damage.

55 nts the development of clinical symptoms and brain damage.

56 infants with MoCD and prevents irreversible brain damage.

57 structural MR imaging markers of subclinical brain damage.

58 napse before the development of irreversible brain damage.

59 rapeutically targeted to minimize poststroke brain damage.

60 causing swelling of the head and potentially brain damage.

61 terious immune responses and limit bystander brain damage.

62 and middle cerebral artery occlusion-induced brain damage.

63 disorder, it can also occur following focal brain damage.

64 ng destructive molecules that may exacerbate brain damage.

65 cerebral ischemia, significantly aggravates brain damage.

66 induced microvascular thrombus formation and brain damage.

67 al therapeutic target to minimize poststroke brain damage.

68 ce of diffuse vascular and neurodegenerative brain damage.

69 ing in postnatal microcephaly with extensive brain damage.

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

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

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

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

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

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

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

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

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

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

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

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

82 ype characterized by increased VWF and worse brain damage after ischemic stroke.

83 euronal excitability and protected mice from brain damage after ischemic stroke.

84 abolished I (Cl,H) in neurons and attenuated brain damage after ischemic stroke.

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

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

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

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

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

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

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

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

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

94 he hippocampus, and the relationship between brain damage and cognitive outcome, are poorly understoo

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

96 Brain damage and functional impairment were reduced by I

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

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

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

100 at immune cells contribute to acute ischemic brain damage and indicate that ischemic inflammation ini

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

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

103 Brain damage and ischemia often trigger cortical spreadi

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

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

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

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

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

109 uria (PKU), a genetic disorder that leads to brain damage and mental retardation if untreated.

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

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

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

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

114 Studies of humans with focal brain damage and non-human animals with experimentally i

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

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

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

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

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

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

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

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

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

124 critical process in post-traumatic secondary brain damage and suggests that PAI-1 may be a central en

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

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

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

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

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

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

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

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

133 1A1 activity that can lead to CNS toxicity, brain damage, and even death.

134 endritic architecture, reduce stroke-induced brain damage, and facilitate functional recovery.

135 attenuates cerebral edema, protects against brain damage, and improves outcomes in a model of stroke

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

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

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

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

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

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

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

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

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

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

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

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

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

149 Brain damage, brain water content, and behavioral assess

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

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

152 ted and these systemic responses may amplify brain damage, but how the injured brain sends out signal

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

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

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

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

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

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

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

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

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

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

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

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

165 Brain damage causing acquired amusia disrupts the functi

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

167 These mice also displayed 13% reduced brain damage compared with wild type.

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

169 g status epilepticus reduces also associated brain damage, delays the development of epilepsy and, wh

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

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

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

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

174 proliferation of cancer cells, and increased brain damage during ischemic stroke.

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

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

177 We investigated whether CD69 was involved in brain damage following an ischemic stroke.

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

179 be a potential therapeutic strategy to limit brain damage following ischemic stroke.

180 lsivity, psychotropic exposure, and possible brain damage from attempts.

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

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

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

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

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

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

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

188 cerebellum is a target of alcoholism-related brain damage in adults, yet no study has prospectively t

189 val in cell culture and severe fever-induced brain damage in affected individuals.

190 Our observations might reflect structural brain damage in areas that are related to cognition; how

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

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

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

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

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

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

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

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

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

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

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

202 Patients with T2DM show brain damage in regions that are involved in cognition,

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

204 38 MAPK activation but also reduces ischemic brain damage in STEP KO mice.

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

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

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

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

209 GN volume as an imaging marker of structural brain damage in these patients.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

228 e ischemic stroke, however it causes further brain damage itself.

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

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

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

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

233 d with oxidative stress-induced vascular and brain damage, mediated by activation of the NADPH oxidas

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

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

236 uch as cancer, diabetes, multiple sclerosis, brain damage, nausea and cardiac disease.

237 Brain damage, neuroinflammation, stroke-induced neurogen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

256 enting of attention in male and female right brain-damaged patients with left spatial neglect.

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

258 In right-brain-damaged patients, neglect severity in the line bis

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

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

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

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

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

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

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

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

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

268 Brain damage resulting in loss of sensory stimulation ca

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

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

271 iases of spatial attention due to unilateral brain damage.SIGNIFICANCE STATEMENT Alpha desynchronizat

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

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

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

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

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

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

278 We show that in patients with right brain damage the pathological enhancement of alpha oscil

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

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

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

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

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

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

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

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

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

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

289 Brain damage was confirmed through intrauterine ultrason

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

291 Ischemic brain damage was measured by determining stroke volume a

292 Using data from patients with focal brain damage, we demonstrate that there is a strong psyc

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

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

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

296 Here, we relate patterns of brain damage with deficits to the content and structure

297 iple sclerosis (MS) has been associated with brain damage with low replicability.

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

299 iousness lasting more than 30 days and focal brain damage within the explored brain regions.

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