ライフサイエンスコーパス: intracerebral

1 ing of HDAC class IIa expression-activity in intracerebral 9L and U87-MG gliomas in rats.

2 increased with time due to interaction with intracerebral Abeta deposits.

3 in barrier of zebrafish larvae and sequester intracerebral Abeta(42) and its elicited toxicity in a n

4 Intracerebral administration of anti-CCL2 antibodies als

5 so blocked in nondepleted mice by continuous intracerebral administration of N-acetylcysteine (NAC),

6 Importantly, intracerebral administration of recombinant OPN into the

7 risk for intracranial bleeding, specifically intracerebral and subarachnoid hemorrhages.

8 (MCA) is the second most common location of intracerebral aneurysms.

9 attributable to a reduced vasodilatation of intracerebral arterioles and is reversible by reducing t

10 and is associated with an increased risk of intracerebral bleeding, especially with the use of antic

11 t viral infection, granuloproliferation, and intracerebral calcification.

12 raventricular adhesions, subependymal cysts, intracerebral calcifications, and microcephaly; however,

13 ons in the brains of diseased mice following intracerebral CWD challenge.

14 from an endemic country who present with an intracerebral cyst.

15 bling task to 10 participants implanted with intracerebral depth electrodes in cortical and subcortic

16 n pattern fully consistent with the reported intracerebral distribution of mGluR2.

17 nd afforded 100% protection against a lethal intracerebral dose of ZIKV (strain MR766).

18 can be evaluated effectively by Stereotactic intracerebral EEG (SEEG).

19 lusion criteria: (i) at least one orthogonal intracerebral electrode contact explored the basal gangl

20 nts submitted to presurgical monitoring with intracerebral electrodes.

21 ence of oscillation entrainment, we analyzed intracerebral electroencephalographic recordings obtaine

22 Intracerebral electroencephalographic recordings with ch

23 We retrospectively investigated the intracerebral electroencephalography (EEG) of patients w

24 to assess the safety and efficacy of a novel intracerebral gene therapy.

25 T1DM had significantly smaller increments in intracerebral glucose levels (P = 0.0002).

26 the occipital lobe to measure the change in intracerebral glucose levels during a 2-h glucose clamp

27 95% CI 1.06 to 1.38) with increased risk of intracerebral haemorrhage (2.07, 95% CI 1.37 to 3.13) an

28 visual acuity (77.8%), headache (16.7%), and intracerebral haemorrhage (5.55%), and 5.55% were asympt

29 published arteriovenous malformation-related intracerebral haemorrhage (AVICH) score showed better ou

30 Patients with primary intracerebral haemorrhage (ICH) are at increased long-te

31 onists oral anticoagulants (NOAC)-associated intracerebral haemorrhage (ICH) are largely unknown.

32 surgical treatment of spontaneous cerebellar intracerebral haemorrhage (ICH) differ.

33 Whether statins increase the risk of intracerebral haemorrhage (ICH) in patients with a previ

34 study, we examined injury progression after intracerebral haemorrhage (ICH) induced by collagenase i

35 Intracerebral haemorrhage (ICH) is a life-threatening em

36 of blood pressure (BP) at the acute phase of intracerebral haemorrhage (ICH) is beneficial.

37 BACKGROUND AND Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, b

38 Intraventricular extension of intracerebral haemorrhage (ICH) predicts poor outcome, b

39 ith arteriovenous malformation (AVM)-related intracerebral haemorrhage (ICH) than other AVM or ICH sc

40 kidney and cerebrovascular disease including intracerebral haemorrhage (ICH), and common collagen IV

41 health-related quality of life (HRQoL) after intracerebral haemorrhage (ICH).

42 ve outcome after spontaneous (non-traumatic) intracerebral haemorrhage (ICH).

43 he incidence of ischaemic stroke (n=14 930), intracerebral haemorrhage (n=3496), and acute myocardial

44 stroke), and outnumbered disabling or fatal intracerebral haemorrhage (n=45 vs n=18), with an absolu

45 % CI = -0.13 to -0.02), but a higher risk of intracerebral haemorrhage (OR: 1.64, 95% CI = 1.26-2.13)

46 ssociation with risk, which was stronger for intracerebral haemorrhage (relative risk [RR] per 280 g

47 While the association between CAA and lobar intracerebral haemorrhage (with its high recurrence risk

48 s 17% ([17-18] ischaemic stroke 16% [15-16], intracerebral haemorrhage 28% [26-29], subarachnoid haem

49 ke at 5 years (ischaemic stroke 41% [41-42], intracerebral haemorrhage 44% [42-46], subarachnoid haem

50 port, we analysed eligible participants with intracerebral haemorrhage according to their treatment a

51 Brain imaging features of intracerebral haemorrhage and cerebral small vessel dise

52 l disease and a largely untreatable cause of intracerebral haemorrhage and contributor to age-related

53 19-99 years with spontaneous (non-traumatic) intracerebral haemorrhage and elevated systolic blood pr

54 gression models for association with primary intracerebral haemorrhage and ischaemic stroke subtypes.

55 Primary intracerebral haemorrhage and lacunar ischaemic stroke a

56 ar instability, leading to increased primary intracerebral haemorrhage and lacunar stroke risk.

57 loperoxidase levels increase risk of primary intracerebral haemorrhage and lacunar stroke, directly i

58 sability, and 8% died - one in the course of intracerebral haemorrhage and one due to other sustained

59 Intracerebral haemorrhage and small vessel ischaemic str

60 icipant eligibility and rate features of the intracerebral haemorrhage and surrounding brain.

61 After combining intracerebral haemorrhage and SVS datasets, our sample s

62 Our cross-phenotype genetic study of intracerebral haemorrhage and SVS demonstrates novel gen

63 lying this novel genome-wide approach across intracerebral haemorrhage and SVS.

64 lator deferoxamine mesylate in patients with intracerebral haemorrhage and to establish whether the d

65 novel genome-wide associations for non-lobar intracerebral haemorrhage at 2q33 and 13q34.

66 or arteriolosclerosis), we performed GWAS of intracerebral haemorrhage by location in 1813 subjects (

67 We used a discovery cohort of 1409 primary intracerebral haemorrhage cases and 1624 controls from t

68 ght reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antipla

69 ght reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antipla

70 nd 138 controls (96 healthy elderly, 42 deep intracerebral haemorrhage controls) and 72 patients with

71 number of outflows and outflow diameter) of intracerebral haemorrhage due to intracranial dural arte

72 ant associations were observed for non-lobar intracerebral haemorrhage enhanced by SVS with rs2758605

73 Intracerebral haemorrhage GWAS results by location were

74 hazards of antiplatelet therapy on recurrent intracerebral haemorrhage in primary subgroup analyses o

75 effect of antiplatelet therapy on recurrent intracerebral haemorrhage in the presence of cerebral mi

76 Acute stroke due to supratentorial intracerebral haemorrhage is associated with high morbid

77 Because intracerebral haemorrhage location is an adequate surrog

78 h spontaneous, non-traumatic, supratentorial intracerebral haemorrhage of 30 mL or more.

79 h favourable outcomes in patients with acute intracerebral haemorrhage of predominantly mild-to-moder

80 patients with CAA versus patients with deep intracerebral haemorrhage or healthy controls.

81 ple size included 241 024 participants (6255 intracerebral haemorrhage or SVS cases and 233 058 contr

82 l haemorrhage survivors for association with intracerebral haemorrhage recurrence.

83 k (odds ratio, 1.07, P = 0.04) and recurrent intracerebral haemorrhage risk (hazards ratio, 1.45, P =

84 ase levels were associated with both primary intracerebral haemorrhage risk (odds ratio, 1.07, P = 0.

85 prespecified baseline covariates (stability intracerebral haemorrhage size, age, Glasgow Coma Scale,

86 odels in a prospective cohort of 174 primary intracerebral haemorrhage survivors for association with

87 e lowering strategies in patients with acute intracerebral haemorrhage to determine the strength of a

88 nd median time from the onset of symptoms of intracerebral haemorrhage to randomisation of 3.6 h (2.7

89 tensive care unit with stable, non-traumatic intracerebral haemorrhage volume less than 30 mL, intrav

90 only and those with frontal infarcts and/or intracerebral haemorrhage were both significantly more l

91 Association estimates for intracerebral haemorrhage were negatively correlated wit

92 rs with primary, spontaneous, supratentorial intracerebral haemorrhage were randomly assigned (1:1) t

93 y participants or patients with non-CAA deep intracerebral haemorrhage) and patients with Alzheimer's

94 ticipants for primary (recurrent symptomatic intracerebral haemorrhage) and secondary (ischaemic stro

95 mplications (cerebrospinal fluid leakage and intracerebral haemorrhage) at days 3-7 after AAV2 gene t

96 evere stroke increasing the absolute risk of intracerebral haemorrhage).

97 CI 3-4) for ischaemic stroke, 47% (46-48)for intracerebral haemorrhage, 19% (17-22; 52% for rural are

98 strokes were also ischaemic stroke; after an intracerebral haemorrhage, 56% of recurrent strokes were

99 troke were ischaemic stroke, 7440 (16%) were intracerebral haemorrhage, 702 (2%) were subarachnoid ha

100 l haemorrhage, 56% of recurrent strokes were intracerebral haemorrhage, and 41% of recurrent strokes

101 ascular disease (including ischaemic stroke, intracerebral haemorrhage, and myocardial infarction) by

102 as on cognition in the context of ageing and intracerebral haemorrhage, as well as in Alzheimer's and

103 2 locus previous seen in traditional GWAS of intracerebral haemorrhage, as well as the rediscovery of

104 they had a structural cerebral cause for the intracerebral haemorrhage, had a low score (3-5) on the

105 For moderate to large intracerebral haemorrhage, MISTIE did not improve the pr

106 Stroke, including acute ischaemic stroke and intracerebral haemorrhage, results in neuronal cell deat

107 iod were recorded by type (ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and

108 Intraventricular haemorrhage is a subtype of intracerebral haemorrhage, with 50% mortality and seriou

109 ong independent risk factor for future lobar intracerebral haemorrhage.

110 e associated with greater risks of recurrent intracerebral haemorrhage.

111 effects of blood pressure lowering in acute intracerebral haemorrhage.

112 who achieved a good response 365 days after intracerebral haemorrhage.

113 improve functional outcome in patients with intracerebral haemorrhage.

114 lood is implicated in secondary injury after intracerebral haemorrhage.

115 50% of patients presented with intracerebral haemorrhage.

116 in patients with probable CAA without lobar intracerebral haemorrhage.

117 traventricular haemorrhage size and thalamic intracerebral haemorrhage.

118 , and loss of functional independence) after intracerebral haemorrhage.

119 o differentiate between ischaemic stroke and intracerebral haemorrhage.

120 rgical interventions are investigational for intracerebral haemorrhage.

121 P = 0.007), older donor age (P = 0.010), and intracerebral haemorrhage/thrombosis in donor (P = 0.023

122 hyperintensities (WMH): 10 597 individuals; intracerebral haemorrhage: 1545 cases, 1481 controls].

123 cipants were enrolled, of whom 525 (98%) had intracerebral haemorrhage: 507 (97%) were diagnosed on C

124 t decreases in DBS complications, with fewer intracerebral haemorrhages and infections with general a

125 embolic events outnumbered warfarin-related intracerebral haemorrhages by about 15-fold (280 vs 19),

126 1384 strokes (1193 ischaemic strokes and 191 intracerebral haemorrhages) in patients admitted during

127 ta on 86 strokes (81 ischaemic strokes and 5 intracerebral haemorrhages) in patients with evidence of

128 bral infarction (TICI) >=2b) and symptomatic intracerebral haemorrhagic (sICH) transformation.

129 No between-group differences of total intracerebral hematoma expansion (%) (median [interquart

130 stroke, aneurysmal subarachnoid hemorrhage, intracerebral hematoma, and trauma.

131 In contrast, rates of intracerebral hemorrhage (6% vs 8%; p = 0.35) did not di

132 type of intracranial hemorrhage, followed by intracerebral hemorrhage (8%), and subdural hemorrhage (

133 and an increased probability of symptomatic intracerebral hemorrhage (adjusted OR per 30 minutes inc

134 ude of association appeared to be higher for intracerebral hemorrhage (HR, 1.9; 95% CI, 1.5-2.4) and

135 Ischemic stroke (IS) and intracerebral hemorrhage (ICH) account for an equal numb

136 Intracerebral hemorrhage (ICH) accounts for a disproport

137 age (IVH) is a negative prognostic factor in intracerebral hemorrhage (ICH) and is associated with pe

138 cal treatment for supratentorial spontaneous intracerebral hemorrhage (ICH) and whether it is modifie

139 sive blood pressure (BP) reduction for acute intracerebral hemorrhage (ICH) are inconsistent.

140 (OAT) resumption is a therapeutic dilemma in intracerebral hemorrhage (ICH) care, particularly for lo

141 giography (CTA) spot sign is associated with intracerebral hemorrhage (ICH) expansion and may mark th

142 e accuracy of using the spot sign to predict intracerebral hemorrhage (ICH) expansion with standardiz

143 linical outcomes in patients with cerebellar intracerebral hemorrhage (ICH) has not been established.

144 onary events (MCE), ischemic stroke (IS) and intracerebral hemorrhage (ICH) in a cohort of Chinese ad

145 Intracerebral hemorrhage (ICH) is a devastating disease

146 Intracerebral hemorrhage (ICH) is a devastating form of

147 Intracerebral hemorrhage (ICH) is a devastating form of

148 Spontaneous deep intracerebral hemorrhage (ICH) is a devastating subtype

149 Intracerebral hemorrhage (ICH) is an especially feared c

150 Intracerebral hemorrhage (ICH) is one of the most devast

151 Concern about intracerebral hemorrhage (ICH) is the primary reason for

152 in injuries (TBIs), multiple sclerosis (MS), intracerebral hemorrhage (ICH), and neuromyelitis optica

153 important modulators of tissue damage after intracerebral hemorrhage (ICH), but how this function is

154 protein (LDL) cholesterol levels and risk of intracerebral hemorrhage (ICH), but it remains unclear w

155 cognitive decline commonly occurs following intracerebral hemorrhage (ICH), but the mechanisms under

156 Following intracerebral hemorrhage (ICH), the activation of mast c

157 MDMs in the murine brain after experimental intracerebral hemorrhage (ICH), we found robust phenotyp

158 itical care might all be beneficial in acute intracerebral hemorrhage (ICH).

159 ccasionally to deliver medications following intracerebral hemorrhage (ICH).

160 pathophysiological mechanisms after onset of intracerebral hemorrhage (ICH).

161 nd tissue diffusion changes in patients with intracerebral hemorrhage (ICH).

162 predictor of poor outcome following an acute intracerebral hemorrhage (ICH).

163 stem cells (BMSCs) transplantation following intracerebral hemorrhage (ICH).

164 uiding treatment in patients presenting with intracerebral hemorrhage (ICH).

165 etamine use has emerged as a risk factor for intracerebral hemorrhage (ICH).

166 .16]; p = 5.3 x 10(-5) ; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84-1.12]

167 To propose and validate a modified pediatric intracerebral hemorrhage (PICH) (mPICH) score and to com

168 . 16.0%, P < 0.001), and similar symptomatic intracerebral hemorrhage (SICH) rates (1.7% vs. 1.8%, P

169 chemic attack/systemic embolism, symptomatic intracerebral hemorrhage (sICH), and major extracranial

170 n in vitro model of hematoma clearance after intracerebral hemorrhage [ICH]), and (3) reduced proinfl

171 ses and 404,630 noncases, and 1,545 cases of intracerebral hemorrhage and 1,481 noncases.

172 A total of 46,735 intracerebral hemorrhage and 331,521 ischemic stroke cas

173 Intracerebral hemorrhage and ischemic stroke admissions

174 determine whether palliative care use after intracerebral hemorrhage and ischemic stroke differs bet

175 Assessment of all-cause mortality of intracerebral hemorrhage and ischemic stroke patients ad

176 sted odds ratio, 0.65; 95% CI, 0.50-0.84 for intracerebral hemorrhage and odds ratio, 0.62; 95% CI, 0

177 ening capillary nets, increasing the risk of intracerebral hemorrhage and stroke.

178 Finally, hospitalization rates for intracerebral hemorrhage and subarachnoid hemorrhage rem

179 t study of adults diagnosed with spontaneous intracerebral hemorrhage between June 1, 2010 and May 31

180 Exclusion criteria included other intracerebral hemorrhage causes, anticoagulation, coagul

181 atrial fibrillation who are also at risk of intracerebral hemorrhage due to cerebral amyloid angiopa

182 inimally Invasive Surgery Plus Alteplase for Intracerebral Hemorrhage Evacuation Phase III trial.

183 Fifty percent of participants with intracerebral hemorrhage experienced augmented renal cle

184 s with aneurysmal subarachnoid hemorrhage or intracerebral hemorrhage experienced enhanced renal clea

185 gist rated the diagnostic brain CT for acute intracerebral hemorrhage features and SVD biomarkers.

186 isability warrant careful prognostication of intracerebral hemorrhage outcomes and should be consider

187 hospital and day-90 SG utilities (SGU) among intracerebral hemorrhage patients and report a 3-way ass

188 puted tomography (CT) perfusion can identify intracerebral hemorrhage patients at high risk of hemato

189 prediction rule for short-term mortality in intracerebral hemorrhage patients but discriminated mort

190 azard ratio, 1.57; 95% CI, 1.39-1.77) and in intracerebral hemorrhage patients compared with these gr

191 Intracerebral hemorrhage patients discharged between Sep

192 ppear to influence palliative care use among intracerebral hemorrhage patients in the United States.

193 val curve gradient among ischemic stroke and intracerebral hemorrhage patients stabilized.

194 From 158 intracerebral hemorrhage patients that underwent MRI, on

195 ride >/= 115 mmol/L) on clinical outcomes in intracerebral hemorrhage patients treated with continuou

196 palliative care for both white and minority intracerebral hemorrhage patients was lower in minority

197 smal subarachnoid hemorrhage patients and 30 intracerebral hemorrhage patients were enrolled, contrib

198 s moderate elevations may impact outcomes in intracerebral hemorrhage patients.

199 Discrimination was affected by study mean Intracerebral Hemorrhage score (beta = -0.05), and calib

200 oducible across cohorts for patients with an Intracerebral Hemorrhage score 0-1 (I = 15%).

201 s (mean age 68.0 [SD 18.4], 62% male, median intracerebral hemorrhage score 1.5 [interquartile range

202 Overall, the Intracerebral Hemorrhage score discriminated well (poole

203 verestimating mortality for patients with an Intracerebral Hemorrhage score greater than 3 (observed:

204 The Intracerebral Hemorrhage score is a valid clinical predi

205 also overestimated mortality in the highest Intracerebral Hemorrhage score patients, with significan

206 easurement, mean study year, and mean cohort Intracerebral Hemorrhage score.

207 ional Institutes of Health Stroke Scale, and intracerebral hemorrhage scores (P<0.001).

208 pans (>= 2) of readings after adjustment for intracerebral hemorrhage severity.

209 61), and (3) the Ethnic/Racial Variations of Intracerebral Hemorrhage study (n = 209).

210 Adult patients with intracerebral hemorrhage under antiplatelet treatment an

211 telet transfusion (2 U) within 60 minutes of intracerebral hemorrhage under antiplatelet treatment di

212 ic efficacy of early platelet transfusion in intracerebral hemorrhage under antiplatelet treatment.

213 Patients with intracerebral hemorrhage underwent in-hospital and day-9

214 Scale scores = 4-6) 1 year after first-ever intracerebral hemorrhage using logistic regression, adju

215 ociation of smoking with ischemic stroke and intracerebral hemorrhage using summary statistics data f

216 ars) and the standardized mortality rate for intracerebral hemorrhage was 8.4 (95% CI, 7.4-9.3; obser

217 hout neurologic symptoms, 6 with prior lobar intracerebral hemorrhage) and 17 mutation noncarriers (M

218 The ERICH study (Ethnic/Racial Variations of Intracerebral Hemorrhage) is a prospective, multicenter,

219 Within 1 year of intracerebral hemorrhage, 224 (56%) of 402 patients died

220 Articles relevant to prognosis in intracerebral hemorrhage, acute ischemic stroke, traumat

221 tients, including 53 with sepsis and 59 with intracerebral hemorrhage, along with 53 control particip

222 direct thrombin inhibitor with a low risk of intracerebral hemorrhage, ameliorates AD pathogenesis in

223 ents, including 10 with sepsis and five with intracerebral hemorrhage, and 11 healthy controls.

224 197% increase (95% CI = 59-457%) in risk of intracerebral hemorrhage, and an increase in white matte

225 , Tenth Revision, codes for ischemic stroke, intracerebral hemorrhage, and stroke not otherwise speci

226 and secondary outcomes were ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage as

227 Delirium is common after intracerebral hemorrhage, but severe neurologic deficits

228 on in patients with both ischemic stroke and intracerebral hemorrhage, especially compared with other

229 onfirmed NHS including primary and secondary intracerebral hemorrhage, hemorrhagic transformation of

230 iated with 1-year death and dependence after intracerebral hemorrhage, independent of known predictor

231 Shortly after intracerebral hemorrhage, neutrophils infiltrate the int

232 h HN improved outcomes in an animal model of intracerebral hemorrhage, suggesting that this process c

233 In patients with intracerebral hemorrhage, there was a higher mean measur

234 rkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischem

235 ebral hemorrhage, neutrophils infiltrate the intracerebral hemorrhage-injured brain.

236 rtality of 31% in ischemic stroke and 42% in intracerebral hemorrhage.

237 essel stroke but not cardioembolic stroke or intracerebral hemorrhage.

238 loci influenced both small vessel stroke and intracerebral hemorrhage.

239 and distal brain region alteration following intracerebral hemorrhage.

240 The most common etiology was intracerebral hemorrhage.

241 upregulated centrally and peripherally after intracerebral hemorrhage.

242 to start or restart anticoagulation after an intracerebral hemorrhage.

243 neurological outcomes in an animal model of intracerebral hemorrhage.

244 it hematoma/iron-mediated brain injury after intracerebral hemorrhage.

245 -0.16%) seizures, and 4% (95% CI, 0.01-0.1%) intracerebral hemorrhage.

246 esponses are associated with the outcomes of intracerebral hemorrhage.

247 they could not be assessed in patients with intracerebral hemorrhage.

248 A TSPO ligand attenuates brain injury after intracerebral hemorrhage.

249 to several clinical complications, including intracerebral hemorrhage.

250 7), but no association with stable angina or intracerebral hemorrhage.

251 tients, including 53 with sepsis and 59 with intracerebral hemorrhage.

252 nslational target for secondary injury after intracerebral hemorrhage.

253 are associated with long-term outcome after intracerebral hemorrhage.

254 , 4,072 with ischemic stroke, and 2,974 with intracerebral hemorrhage.

255 "beneficial" phenotype for the treatment of intracerebral hemorrhage.Neutrophils are important modul

256 Small focal intracerebral hemorrhages only visible on exquisitely se

257 A majority of patients (20 of 37, 54%) had intracerebral hemorrhagic lesions with a more severe cli

258 challenges of goats with scrapie by both the intracerebral (i.c.) and oral routes, exploring the effe

259 In response to intracerebral (I.C.) injection of Daniel's (DA) strain o

260 Administration of human neural stem cells by intracerebral implantation is feasible in a multicentre

261 We investigated the feasibility of intracerebral implantation of the allogeneic human neura

262 ld-type and marker-rescued viruses following intracerebral infection.

263 flammatory eicosanoid expression, influences intracerebral inflammation, and predicts survival from T

264 ing exerts additive effects in orchestrating intracerebral inflammation, leading to the development o

265 , while killing the bacteria and controlling intracerebral inflammation.

266 characterized the pretreatment clinical and intracerebral inflammatory phenotype and 9-month surviva

267 S. stercoralis co-infection may modulate the intracerebral inflammatory response to M. tuberculosis a

268 Moreover, direct intracerebral infusion of FGF20 protects against nigrost

269 expressing DREADDs was paired with localized intracerebral infusions of a ligand to target specific i

270 he templated aggregation of soluble tau upon intracerebral injection into tau transgenic (Tg) and wil

271 Tau activated the NLRP3 inflammasome and intracerebral injection of fibrillar amyloid-beta-contai

272 Of note, intracerebral injection of RAGE antibody into the hippoc

273 The intracerebral injection of S. pneumoniae D39 induced the

274 Intracerebral injection of tau aggregates isolated from

275 In mice, the intracerebral injection of Tau inclusions induces the or

276 We have previously shown that after intracerebral injection, antigen-loaded bone marrow DC m

277 Intracerebral injections of distinct human tauopathy bra

278 However, intracerebral injections of either T40PL preformed fibri

279 PO, devoid of viral neuropathogenicity after intracerebral inoculation in human subjects, for stable

280 Here, we performed intracerebral inoculation of embryonic mouse brains with

281 Neurovirulence following intracerebral inoculation of mice was not affected by th

282 mice (Tg40h) at different time points after intracerebral inoculation with 263K and sCJDMM1 prions,

283 Using intracerebral inoculation with MuPyV, we found that MuPy

284 tion is inducible in rodents and primates by intracerebral inoculation.

285 A retrospective review of 597 intracerebral malformation embolisations yielded 40 embo

286 We addressed these issues by combining intracerebral microinfusions with cardiovascular and beh

287 By combining targeted intracerebral microinfusions with cardiovascular and beh

288 Additionally, intracerebral microinjection of pathologic tau led to in

289 ggregation in alphaS transgenic mice through intracerebral or peripheral injection of various mutant

290 =1.53; 95% CI, 1.31-1.78; P=3.32x10(-8)) and intracerebral (OR=1.34; 95% CI, 1.14-1.58; P=4.05x10(-4)

291 INTERPRETATION: Intracerebral rAVV2/5 was well tolerated and induced sus

292 We show, using human intracerebral recordings, that 100-400 Hz high-frequency

293 Purpose To evaluate the ability to detect intracerebral regions of increased glucose concentration

294 athological data that inflammation-dependent intracerebral remodeling of the vessel wall is directly

295 and clearance, are juxtaposed to the wall of intracerebral resistance vessels and are a powerful sour

296 es (e.g., transcranial magnetic stimulation, intracerebral stem/progenitor cells) that consider preci

297 Patients with intracerebral, subarachnoid, or subdural hemorrhages who

298 Intracerebral Theiler's murine encephalomyelitis virus (

299 meningeal and dermal vessels were affected, intracerebral vessels, which are known for their tighter

300 long-range compared to mid- and short-range intracerebral white matter fibres; and (ii) the number o