ライフサイエンスコーパス: intracerebral

1 the ability of prions to infect the host via intracerebral administration depends on PrP(Sc) sialylat

2 Intracerebral administration of anti-CCL2 antibodies als

3 ent to prime microglia, IS was replaced with intracerebral administration of disulfide or fully reduc

4 Importantly, intracerebral administration of recombinant OPN into the

5 Upon intracerebral administration, all animals that received

6 ood pressure effects after both systemic and intracerebral administrations.

7 d all the clinical manifestations induced by intracerebral bipolar electrical stimulation in 172 pati

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

9 t viral infection, granuloproliferation, and intracerebral calcification.

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

11 ve late-lethal mutant that lacks most of the intracerebral central arteries (CtAs), but not other bra

12 celerated T cell influx into the brain after intracerebral challenge of vaccinated mice, and this T c

13 are dispensable for long-term survival after intracerebral challenge.

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

15 Intracerebral delivery of JCV resulted in infection and

16 tion between neurodegenerative disorders and intracerebral deposition of polyglutamine aggregates mot

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

18 Intracerebral disulfide HMGB-1 mimicked the effect of th

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

20 Single intracerebral doses of CTX-DP up to 20 million cells ind

21 c brain regions, explaining the responses to intracerebral electric stimulation in epileptogenic and

22 firmed in human focal seizures recorded with intracerebral electrodes in patients with drug-resistant

23 Here, using intracerebral electrodes sampling the human motor cortex

24 nts submitted to presurgical monitoring with intracerebral electrodes.

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

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

27 chaemic stroke (1.68, 95% CI 1.60-1.77), and intracerebral haemorrhage (1.24, 95% CI 1.07-1.44).

28 lic blood pressure was much lower than after intracerebral haemorrhage (158.5 mm Hg [SD 30.1] vs 189.

29 eeded the absolute increase in risk of fatal intracerebral haemorrhage (2.2% [1.5% to 3.0%]) and the

30 bsolute excess 3.1% [2.4-3.8]); and of fatal intracerebral haemorrhage (91 [2.7%] of 3391 vs 13 [0.4%

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

32 Neither incidence of symptomatic intracerebral haemorrhage (by SITS-MOST definition, 1/52

33 h systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1.44 [95% CI 1.3

34 Antithrombotic agents increase risks of intracerebral haemorrhage (ICH) and associated adverse o

35 ERACT2 enrolled 2839 adults with spontaneous intracerebral haemorrhage (ICH) and high systolic blood

36 the relationship between laterality of acute intracerebral haemorrhage (ICH) and poor clinical outcom

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

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

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

40 Poor prognosis after intracerebral haemorrhage (ICH) is related to haemorrhag

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

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

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

44 ion rate may be a predictor of outcome after intracerebral haemorrhage (ICH).

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

46 id angiopathy (CAA) is associated with lobar intracerebral haemorrhage (ICH).

47 ut the long-term prognosis after spontaneous intracerebral haemorrhage (ICH).

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

49 than two times higher in patients with lobar intracerebral haemorrhage (incidence at 1 year 23.4%, 14

50 14.6-33.3) than for patients with non-lobar intracerebral haemorrhage (incidence at 1 year 9.2%, 5.1

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

52 racerebral haemorrhage from the Prognosis of Intracerebral Haemorrhage (PITCH) cohort who were admitt

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

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

55 ed cerebral small vessel disorder leading to intracerebral haemorrhage and dementia.

56 ploratory analyses to assess mortality after intracerebral haemorrhage and examine the absolute risks

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

58 Primary intracerebral haemorrhage and lacunar ischaemic stroke a

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

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

61 cerebrovascular permeability, development of intracerebral haemorrhage and neurovascular injury in ex

62 Delayed seizures after intracerebral haemorrhage are associated with different

63 are alone, reduced death or dependence after intracerebral haemorrhage associated with antiplatelet t

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

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

66 From the 560 patients with spontaneous intracerebral haemorrhage enrolled in the PITCH cohort b

67 n, 3/52 [6%] vs 4/51 [8%], p=0.59) nor total intracerebral haemorrhage events (8/52 [15%] vs 14/51 [2

68 al cohort study in patients with spontaneous intracerebral haemorrhage from the Prognosis of Intracer

69 transfusion after acute spontaneous primary intracerebral haemorrhage in people taking antiplatelet

70 aemorrhage and examine the absolute risks of intracerebral haemorrhage in the context of functional o

71 e interventions (seizure after discharge and intracerebral haemorrhage in the recreational activity g

72 ke severity, but the absolute excess risk of intracerebral haemorrhage increased with increasing stro

73 prespecified subgroup analysis, according to intracerebral haemorrhage location.

74 Late seizures after intracerebral haemorrhage occur after the initial acute

75 -80 years with a non-traumatic (spontaneous) intracerebral haemorrhage of 20 mL or higher to standard

76 tratified by trial, to model the log odds of intracerebral haemorrhage on allocation to alteplase, tr

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

78 l haemorrhage survivors for association with intracerebral haemorrhage recurrence.

79 eria were pure intraventricular haemorrhage; intracerebral haemorrhage resulting from intracranial va

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

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

82 djusted for stratification variables and the Intracerebral Haemorrhage Score.

83 ture clinical trials including patients with intracerebral haemorrhage should assess cognitive endpoi

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

85 ective longitudinal follow-up of consecutive intracerebral haemorrhage survivors presenting to a sing

86 enrolled adults within 6 h of supratentorial intracerebral haemorrhage symptom onset if they had used

87 Hypertension was more associated with intracerebral haemorrhage than with ischaemic stroke, wh

88 ever, the risk of dementia after spontaneous intracerebral haemorrhage that accounts for about 15% of

89 th increasing stroke severity: for SITS-MOST intracerebral haemorrhage the absolute excess risk range

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

91 e-phase blood pressure reading after primary intracerebral haemorrhage was more likely than after isc

92 owever defined, the proportional increase in intracerebral haemorrhage was similar irrespective of tr

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

94 A total of 872 survivors of intracerebral haemorrhage were enrolled and followed for

95 s of Health Stroke Scale [NIHSS]); and fatal intracerebral haemorrhage within 7 days.

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

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

98 ital with acute stroke (ischaemic or primary intracerebral haemorrhage) in England and Wales between

99 dwide (91.5% for ischaemic stroke, 87.1% for intracerebral haemorrhage), and were consistent across r

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

101 of 14.2% (95% CI 10.0-19.3) at 1 year after intracerebral haemorrhage, and incidence reached 28.3% (

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

103 alteplase seems to be safe in patients with intracerebral haemorrhage, but increased asymptomatic bl

104 bsolute effects of alteplase on the risks of intracerebral haemorrhage, mortality, and functional imp

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

106 st an association with a high risk of future intracerebral haemorrhage, with potential implications f

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

108 idence of dementia and risk factors after an intracerebral haemorrhage.

109 es on long-term functional performance after intracerebral haemorrhage.

110 ally invasive surgery (MIS) in patients with intracerebral haemorrhage.

111 cal management as a therapeutic strategy for intracerebral haemorrhage.

112 or people taking antiplatelet therapy before intracerebral haemorrhage.

113 s, does not improve functional outcome after intracerebral haemorrhage.

114 complications and no increase in symptomatic intracerebral haemorrhage.

115 redict a poor outcome in patients with acute intracerebral haemorrhage.

116 in patients with probable CAA without lobar intracerebral haemorrhage.

117 traventricular haemorrhage size and thalamic intracerebral haemorrhage.

118 ified assessment of three classifications of intracerebral haemorrhage: type 2 parenchymal haemorrhag

119 ia in dementia-free survivors of spontaneous intracerebral haemorrhage; our results suggest that unde

120 owever, alteplase also increases the risk of intracerebral haemorrhage; we aimed to determine the pro

121 cases [10 388 with ischaemic stroke and 3059 intracerebral haemorrhage] and 13 472 controls).

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

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

124 9-60) in 2013; symptomatic post-thrombolysis intracerebral haemorrhages occurred in 28 of 675 patient

125 Thus, idarucizumab prevents excess intracerebral hematoma formation in mice anticoagulated

126 Pretreatment with DE increased intracerebral hematoma volume and cerebral hemoglobin co

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

128 ge (32%), and 1,404 ventilated patients with intracerebral hemorrhage (49%) of whom 1,084 (38%) were

129 in Alzheimer disease (chr2p21 and chr10q24), intracerebral hemorrhage (chr1q22), neuroinflammatory di

130 ellar microbleeds) were at increased risk of intracerebral hemorrhage (hazard ratio, 5.27; 95% confid

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

132 s further divided into those with past lobar intracerebral hemorrhage (ICH) (n = 21) and those with c

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

134 Patients who have experienced intracerebral hemorrhage (ICH) appear to develop cogniti

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

136 Transient symptoms from an intracerebral hemorrhage (ICH) are not well recognized a

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

138 ortant determinant of outcome in spontaneous intracerebral hemorrhage (ICH) due to small vessel disea

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

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

141 oding a collagen-binding Cnm protein induced intracerebral hemorrhage (ICH) experimentally and was al

142 of these markers for the differentiation of intracerebral hemorrhage (ICH) from ischemic stroke (IS)

143 The role of CD47 in intracerebral hemorrhage (ICH) has not been investigated

144 Intracerebral hemorrhage (ICH) is a devastating disease

145 Intracerebral hemorrhage (ICH) is a devastating form of

146 Intracerebral hemorrhage (ICH) is a devastating type of

147 Persistent intracerebral hemorrhage (ICH) is a major cause of death

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

149 Intracerebral hemorrhage (ICH) is the most devastating a

150 Intracerebral hemorrhage (ICH) is the most severe form o

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

152 ma, and improves neurological function in an intracerebral hemorrhage (ICH) mouse model.

153 of specific antidotes is a major concern in intracerebral hemorrhage (ICH) related to direct anticoa

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

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

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

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

158 ypertension is a significant risk factor for intracerebral hemorrhage (ICH).

159 rove long-term functional outcomes following intracerebral hemorrhage (ICH).

160 nd may play a role in the pathophysiology of intracerebral hemorrhage (ICH).

161 ) has been associated with increased risk of intracerebral hemorrhage (ICH).

162 erebral microbleeds, porencephaly, and fatal intracerebral hemorrhage (ICH).

163 lack of data on how to treat OAC-associated intracerebral hemorrhage (ICH).

164 ts of TSC were also tested in a rat model of intracerebral hemorrhage (ICH).

165 use has a similar effect among patients with intracerebral hemorrhage (ICH).

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

167 = .04) and CAA presentation with symptomatic intracerebral hemorrhage (odds ratio, 2.23; 95% CI, 1.07

168 weeks) who had additional increased odds of intracerebral hemorrhage (OR = 1.84; 95% CI, 1.11-3.03)

169 .16]; p = 5.3 x 10(-5) ; N = 3,670), but not intracerebral hemorrhage (OR [95% CI] = 0.97 [0.84-1.12]

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

171 Treatments for symptomatic intracerebral hemorrhage (sICH) are based on expert opin

172 n of CMB burden with the risk of symptomatic intracerebral hemorrhage (sICH) in patients with acute i

173 The primary safety outcome was symptomatic intracerebral hemorrhage (sICH) with preplanned stopping

174 reatment is thrombolysis-related symptomatic intracerebral hemorrhage (sICH), which occurs in nearly

175 MO deployment incurred no increased risk for intracerebral hemorrhage (STEMO deployment: 7/200; conve

176 subarachnoid hemorrhage 0.17 (0.06-0.45) and intracerebral hemorrhage 0.57 (0.34-0.94).

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

178 r CMBs were similar to those for symptomatic intracerebral hemorrhage and differed for lobar and deep

179 Intracerebral hemorrhage and ischemic stroke admissions

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

181 Hematoma expansion occurs in children with intracerebral hemorrhage and may require urgent treatmen

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

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

184 tilization of palliative care in spontaneous intracerebral hemorrhage at a population level using a l

185 Symptomatic intracerebral hemorrhage based on the European Cooperati

186 o, 1.23; 95% CI, 1.18-1.30; p < 0.001), high intracerebral hemorrhage case volume (p < 0.001), antico

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

188 All 5 patients with an intracerebral hemorrhage had lobar microbleeds at baseli

189 sing trend of palliative care utilization in intracerebral hemorrhage has occurred over the last deca

190 Intracerebral hemorrhage is a devastating disorder with

191 Symptomatic intracerebral hemorrhage occurred in 3.6% of participant

192 e evidence to guide treatment strategies for intracerebral hemorrhage on vitamin K antagonists (VKA-I

193 Worthwhile interventions for intracerebral hemorrhage or subarachnoid hemorrhage gene

194 Intracerebral hemorrhage patients discharged between Sep

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

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

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

198 Intracerebral hemorrhage patients with and without palli

199 Of the 311,217 intracerebral hemorrhage patients, 32,159 (10.3%) receiv

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

201 ncy, (4) status post cardiac arrest, and (5) intracerebral hemorrhage requiring mechanical ventilatio

202 ed after adjusting for all components of the intracerebral hemorrhage score (odds ratio, 2.21; 95% CI

203 sociation persisted after adjustment for all intracerebral hemorrhage score components (odds ratio, 2

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

205 linical role of hyperoxemia in patients with intracerebral hemorrhage treated in the ICU remains cont

206 No statistical difference in symptomatic intracerebral hemorrhage was found (5.6% vs 2.1% for the

207 sion protects blood-brain barrier(BBB) after intracerebral hemorrhage(ICH) remains unexplored.

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

209 mbolysis, 7- and 90-day mortality, secondary intracerebral hemorrhage, and discharge home.

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

211 d ratio <1.5) for transient ischemic attack, intracerebral hemorrhage, and unstable angina, and inver

212 Three days after intracerebral hemorrhage, brain edema, hematoma volume a

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

214 Intracerebral hemorrhage, intraventricular hemorrhage, a

215 stroke (HS), ie, subarachnoid hemorrhage and intracerebral hemorrhage, is more common than ischemic s

216 rebral arteries and is an important cause of intracerebral hemorrhage, ischemic stroke, and cognitive

217 Shortly after intracerebral hemorrhage, neutrophils infiltrate the int

218 the WARCEF primary outcome (ischemic stroke, intracerebral hemorrhage, or death), with death alone, i

219 verse events (AEs), including death, stroke, intracerebral hemorrhage, pericardial complications, hem

220 (CMBs), which are asymptomatic precursors of intracerebral hemorrhage, reflects specific underlying m

221 the newborn, infective pneumonia, asphyxia, intracerebral hemorrhage, seizure, cardiomyopathy, periv

222 the final vascular events (brain infarction, intracerebral hemorrhage, subarachnoid hemorrhage, coron

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

224 ical," "stroke," "subarachnoid hemorrhage," "intracerebral hemorrhage," or "brain injury." DATA EXTRA

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

226 nslational target for secondary injury after intracerebral hemorrhage.

227 come); the secondary outcome was symptomatic intracerebral hemorrhage.

228 edema expansion rate predicts outcome after intracerebral hemorrhage.

229 upregulated centrally and peripherally after intracerebral hemorrhage.

230 n increased risk of both ischemic stroke and intracerebral hemorrhage.

231 roke-related mortality, incident stroke, and intracerebral hemorrhage.

232 differences in rates of death or symptomatic intracerebral hemorrhage.

233 to start or restart anticoagulation after an intracerebral hemorrhage.

234 n mortality or the occurrence of symptomatic intracerebral hemorrhage.

235 may increase the development or severity of intracerebral hemorrhage.

236 neurological outcomes in an animal model of intracerebral hemorrhage.

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

238 esponses are associated with the outcomes of intracerebral hemorrhage.

239 A TSPO ligand attenuates brain injury after intracerebral hemorrhage.

240 to several clinical complications, including intracerebral hemorrhage.

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

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

243 Other endpoints included: asymptomatic intracerebral hemorrhage; clinical improvement in NIHSS;

244 xerts protective effects in a mouse model of intracerebral hemorrhage; the mechanisms underlying thes

245 the wall), clinical presentation, number of intracerebral hemorrhages, and other imaging markers not

246 increased bleeding complications, including intracerebral hemorrhages.

247 Intracerebral hemorrhagic stroke and vascular dementia a

248 (SRF), suffer from loss of BBB integrity and intracerebral hemorrhaging.

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

250 state had near-wild-type virulence following intracerebral infection of STING(-/-) mice.

251 Intracerebral infection with the neurotropic JHM strain

252 Intracerebral infection with Theiler's murine encephalom

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

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

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

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

257 Moreover, upon intracerebral infusion along with the local application

258 nt, focal blockade of glutamate receptors by intracerebral infusion of kynurenic acid.

259 Furthermore, the localized intracerebral infusion of Nrp1- or Sema3A-neutralizing a

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

261 g protein fragment complementation assay and intracerebral injection of alpha-synuclein and SOD1 seed

262 Intracerebral injection of amyloidogenic alpha-synuclein

263 Microglial depletion by intracerebral injection of liposome-encapsulated clodron

264 pal neurons is prevented dose-dependently by intracerebral injection of NAD(+).

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

266 nsgenic mice (line M20), we demonstrate that intracerebral injection of recombinant amyloidogenic or

267 The intracerebral injection of S. pneumoniae D39 induced the

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

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

270 Here we performed intracerebral injections of alpha-syn-containing prepara

271 However, intracerebral injections of either T40PL preformed fibri

272 HSCs induced cerebral beta-amyloidosis upon intracerebral inoculation into young APP tg mice.

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

274 Using intracerebral inoculation of embryonic mouse brains, we

275 In this study, we found that intracerebral inoculation of tau fibrils purified from A

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

277 duce detectable disease in infant mice after intracerebral inoculation.

278 following subcutaneous, intraperitoneal, or intracerebral inoculation.

279 on of TGFbr2/ALK5 signaling in microglia via intracerebral liposome-encapsulated SB-431542 delivery t

280 Intracerebral microdialysis revealed a lower level of ac

281 ctivity within the CeA or BLA in macaques by intracerebral microinjection of muscimol (to inactivate)

282 losis treatment would enhance the killing of intracerebral Mycobacterium tuberculosis organisms and d

283 n vivo in mice predisposed to SCA1 following intracerebral oligomeric tissue inoculation.

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

285 mic stroke, but not in control patients with intracerebral or subarachnoid hemorrhage.

286 nerative conditions are characterized by the intracerebral presence of Lewy bodies, containing amyloi

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

288 combines anatomical and functional data from intracerebral recordings of nearly 100 patients, to gene

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

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

291 ath identified at autopsy, no MR, and scanty intracerebral sequestration.

292 mples were categorized as either spontaneous intracerebral, spontaneous subdural, or postoperative.

293 Intracerebral Theiler's murine encephalomyelitis virus (

294 Concomitantly, intracerebral thrombosis [assessed by fibrin(ogen) depos

295 Reduced intracerebral thrombosis and improved cerebral blood flo

296 Intracerebral tumors as small as 2-3 mm also were clearl

297 cell arteritis, granulomatous aortitis, and intracerebral varicella zoster virus (VZV) vasculopathy.

298 way that acts in endothelial cells to enable intracerebral vascularization and proper expression of m

299 lation in coronal sections in response to an intracerebral ventricular injection of leptin.

300 Because intracerebral VZV vasculopathy and giant cell arteritis