ライフサイエンスコーパス: brain parenchyma

1 ood, peripheral tissues, BBB endothelium and brain parenchyma).

2 brain, leading to a mass of blood within the brain parenchyma.

3 large reservoir of less soluble Abeta(42) in brain parenchyma.

4 MRL/lpr) lupus mice by IgG infiltration into brain parenchyma.

5 te antigens localized selectively within the brain parenchyma.

6 plaque load, or levels of insoluble Abeta in brain parenchyma.

7 their cognate signaling pathways within the brain parenchyma.

8 stablishment and growth of metastases in the brain parenchyma.

9 tumor growth and invasion of the surrounding brain parenchyma.

10 r determinant of melanoma cell growth in the brain parenchyma.

11 particle localisation is observed within the brain parenchyma.

12 integrity and as such, glioma invasion into brain parenchyma.

13 brain injury, albumin may gain access to the brain parenchyma.

14 , and no HSV antigens were detectable in the brain parenchyma.

15 srupted BBB and diffusely distributed in the brain parenchyma.

16 n brain capillaries than those in the CP and brain parenchyma.

17 ctivity on magnetic resonance imaging in the brain parenchyma.

18 n cancer cells while sparing the surrounding brain parenchyma.

19 that 49% of the (131)I-P-GUS in brain was in brain parenchyma.

20 y infiltrate the tumor from the blood or the brain parenchyma.

21 only as diffuse non-fibrillar plaques in the brain parenchyma.

22 tment for isolated CNS relapse involving the brain parenchyma.

23 cur in two locations, namely the pia and the brain parenchyma.

24 ivation in situ of bona fide pDCs within the brain parenchyma.

25 ytoid DCs (pDCs; >50-fold; p < 0.001) to the brain parenchyma.

26 nd microglial/macrophage accumulation in the brain parenchyma.

27 nels facilitate convective transport through brain parenchyma.

28 crophages and dendritic cells (DCs) into the brain parenchyma.

29 ) facilitates water movement into and out of brain parenchyma.

30 and a transitional zone (Layer IV) into the brain parenchyma.

31 as well as thioflavine S-positive plaques in brain parenchyma.

32 ctively binds to glioma cells but not normal brain parenchyma.

33 the distribution of the radiolabeled mAb in brain parenchyma.

34 mechanism of convective solute transport in brain parenchyma.

35 tes perform surveillance functions in normal brain parenchyma.

36 atio of Abeta 40:42 was elevated relative to brain parenchyma.

37 , is lower than in the adjacent, tumour-free brain parenchyma.

38 ammatory responses to dying parasites in the brain parenchyma.

39 ing the peak of T-cell infiltration into the brain parenchyma.

40 in vascular endothelial cells throughout the brain parenchyma.

41 emigrate preferentially into ischemic cortex brain parenchyma.

42 ated by the accumulation of serum IgG in the brain parenchyma.

43 e for the presence of this connexin in adult brain parenchyma.

44 hat inhibit the accumulation of Abeta in the brain parenchyma.

45 h occasional members interspersed throughout brain parenchyma.

46 h microglia and astrocytes in plaques in the brain parenchyma.

47 ancer cell adhesion and trafficking into the brain parenchyma.

48 ocytes and a population of astrocytes in the brain parenchyma.

49 the brain and meninges, and extends into the brain parenchyma.

50 It is converted in AD to a fibrillar form in brain parenchyma.

51 11-specific CD4+ T cells was detected in the brain parenchyma.

52 ere blocked only partially from entering the brain parenchyma.

53 o CD8+ T cells, few CD4+ T cells entered the brain parenchyma.

54 have eluded regional localization within the brain parenchyma.

55 oss the BBB of mice in vivo to arrive at the brain parenchyma.

56 quinolinic acid levels with those in CSF and brain parenchyma.

57 formed with invasion of tumor cells into the brain parenchyma.

58 pH was placed through a left-side bolt into brain parenchyma.

59 pillaries resulting in the protection of the brain parenchyma.

60 but was essential for trafficking within the brain parenchyma.

61 the detectable tumor and in the surrounding brain parenchyma.

62 he case of capillaries) immediately adjacent brain parenchyma.

63 are being developed to remove Abeta from the brain parenchyma.

64 s presented as remarkably softer than normal brain parenchyma.

65 ystemically circulated tracer leaks into the brain parenchyma.

66 xchange between the subarachnoid CSF and the brain parenchyma.

67 nt, characterized by diffuse invasion of the brain parenchyma.

68 d an overall complete response in CSF and/or brain parenchyma.

69 eal compartment compared with the underlying brain parenchyma.

70 and flow of cerebrospinal fluid outside the brain parenchyma.

71 ebral lateral ventricle and infection of the brain parenchyma.

72 and accumulate in a perivascular zone of the brain parenchyma.

73 T-cell and trypanosoma infiltration into the brain parenchyma.

74 dothelial cells, whereas 30% were within the brain parenchyma.

75 hree-point ordinal scale (0 = hypointense to brain parenchyma, 1 = isointense to brain parenchyma, 2

76 tense to brain parenchyma, 1 = isointense to brain parenchyma, 2 = hyperintense to brain parenchyma)

77 in brain vessels, perivascular cells and in brain parenchyma 30 min after intravenous injection.

78 generally infiltrate the surrounding normal brain parenchyma, a process associated with increased va

79 lenge in the TMEV model is directly into the brain parenchyma, a site that is considered immune privi

80 o extracellular beta-amyloid deposits in the brain parenchyma (Abeta plaques) and in the vasculature

81 iffers substantially from humans because the brain parenchyma accumulates numerous, diffuse, nonfibri

82 cular organs and disseminated throughout the brain parenchyma, accumulating on the plasma membranes o

83 injected via a double-injection cannula into brain parenchyma adjacent to the MCA of anesthetized rat

84 We next demonstrated peptide delivery to the brain parenchyma after in vivo delivery by detecting bio

85 nhanced tumor cell dissemination in adjacent brain parenchyma after ionizing radiation (IR).

86 ition, we showed hemoglobins penetrated into brain parenchyma after SAH.

87 opic fungus Cryptococcus neoformans into the brain parenchyma after systemic infection.

88 ary structure and labels amyloid in both the brain parenchyma (amyloid plaques) and blood vessels.

89 tein (Abeta) fibrils into plaques within the brain parenchyma and along cerebral blood vessels is a h

90 plex staining by immunohistochemistry in the brain parenchyma and barely detectable levels of viral n

91 lele, Abeta was effectively cleared from the brain parenchyma and brain microglial activation was red

92 anti-Abeta antibodies to deposited Abeta in brain parenchyma and CAA.

93 of studied radiolabelled f-MWNT in the whole brain parenchyma and capillaries while 3D-single photon

94 is the deposition of amyloid beta (Abeta) in brain parenchyma and cerebral blood vessels, accompanied

95 us indirectly to the amyloid deposits of the brain parenchyma and cerebral blood vessels.

96 s of the beta-amyloid peptide (Abeta) in the brain parenchyma and cerebral blood vessels.

97 mulate in Alzheimer disease in both affected brain parenchyma and cerebral vasculature.

98 the accumulation of amyloid beta (Abeta) in brain parenchyma and cerebral vasculature.

99 a role for UII/URP at the interface between brain parenchyma and cerebrospinal fluid.

100 ition of the Abeta peptides deposited in the brain parenchyma and cerebrovascular walls of triple tra

101 rce of enzyme secretion into the surrounding brain parenchyma and CSF.

102 calization of klotho mRNA and protein in rat brain parenchyma and demonstrate that klotho levels vary

103 have a distinctive ability to infiltrate the brain parenchyma and disrupt the neural extracellular ma

104 ce astroglial scarring at boundaries between brain parenchyma and fluids, and at junctions between gr

105 inear discriminant model used to distinguish brain parenchyma and gliomas yielded an overall sensitiv

106 a further assisted in discrimination between brain parenchyma and gliomas.

107 of cerebrospinal fluid CD4 T cells into the brain parenchyma and highlight implications on brain imm

108 eposition of beta-amyloid (Abeta) within the brain parenchyma and its subsequent accumulation into se

109 43 are the main Abeta peptides deposited in brain parenchyma and LMD-CWPs in association with the PS

110 letal level, which enables it to protect the brain parenchyma and maintain a homeostatic environment.

111 ation of SIV RNA-positive giant cells in the brain parenchyma and meninges.

112 s yet unclear whether and how they enter the brain parenchyma and migrate to target specific Ags.

113 ogist's review of the imaging studies of the brain parenchyma and of the degree of carotid stenosis,

114 lecules (PBAE-PEG) rapidly penetrate healthy brain parenchyma and orthotopic brain tumor tissues in r

115 were found in increased numbers in both the brain parenchyma and perivascular spaces of pre-AIDS bra

116 creased numbers of B lymphocytes in both the brain parenchyma and perivascular spaces.

117 al differences between anatomical regions of brain parenchyma and secondary infiltration.

118 eripheral cytokine interleukin-6 (IL-6) into brain parenchyma and subsequent expression of depression

119 tricular organs at the interface between the brain parenchyma and the blood-brain barrier.

120 e levels of virus were also found within the brain parenchyma and the cerebrospinal fluid (CSF), with

121 tissue staining for CNPS was detected in the brain parenchyma and the meninges in all cases.

122 cts of long term implantation on surrounding brain parenchyma and the resulting alterations in the fu

123 erapeutic polypeptides from the blood to the brain parenchyma and thus hinders effective treatment of

124 es of individual beta-amyloid plaques in the brain parenchyma and vasculature and requires no stainin

125 showed increased superoxide formation in the brain parenchyma and vasculature during reperfusion.

126 accumulate in association with cells of the brain parenchyma and vasculature.

127 the amyloid deposited extracellularly in the brain parenchyma and vessel walls is amyloid beta-protei

128 constituent of the amyloid deposited in the brain parenchyma and vessel walls of Alzheimer's disease

129 ed in increases in mAb (P < 0.05) in plasma, brain parenchyma, and cerebrospinal fluid and decreases

130 Binding to microvessels, transport into brain parenchyma, and choroidal uptake of both apoJ and

131 factor (CNTF), direct injection of CNTF into brain parenchyma, and ectopic expression of CNTF by an a

132 vary on where klotho is expressed within the brain parenchyma, and no data is available as to whether

133 R amyloid deposits in the leptomeninges, the brain parenchyma, and the eye.

134 r (BBB) provides limited immune privilege to brain parenchyma, and the immune response to recombinant

135 or cells disperse extensively throughout the brain parenchyma, and the need for tumor-specific drug t

136 s of both 45 nm and 80 nm diameter reach the brain parenchyma, and their accumulation there (visualiz

137 hly ramified processes constantly survey the brain parenchyma, and they respond promptly to brain dam

138 sponse, namely, professional APCs within the brain parenchyma, and this could counteract the intrinsi

139 virus, which was directly injected into the brain parenchyma, and to determine whether this response

140 As the normal brain parenchyma appears to have either low-density or a

141 F virus as a surrogate for virus activity in brain parenchyma are not well established.

142 cause prolonged increases in 2-AG amounts in brain parenchyma are thought to orchestrate neuroinflamm

143 hen the amount of A beta is increased in the brain parenchyma as a result of either overexpression or

144 patients with isolated CNS relapse with the brain parenchyma as initial relapse site were eligible.

145 y amyloid-beta (Abeta) peptide deposition in brain parenchyma as plaques and in cerebral blood vessel

146 Abeta depositions in brain parenchyma as senile plaques and along cerebrovasc

147 tion despite a paucity of spirochetes in the brain parenchyma at times of high bacteremia.

148 e widespread distribution of therapeutics in brain parenchyma away from the point of local administra

149 C. neoformans was found in the brain parenchyma away from the vessels by 22 h.

150 y conventional radiological modalities, i.e. brain parenchyma, bones and extremities, can be evaluate

151 tis and perivascular cuffing not only in the brain parenchyma but also in the spinal cord, with no ev

152 marked decrease in plaque deposition in the brain parenchyma but an equally striking increase in CAA

153 ells significantly reduced metastasis to the brain parenchyma but did not induce metastasis to the le

154 2 reduction decreased amyloid plaques in the brain parenchyma but promoted the development of cerebro

155 uently dissociates from transferrin to enter brain parenchyma by an unknown mechanism.

156 h quantifies biomechanical properties of the brain parenchyma by analyzing the propagation of externa

157 Mecp2-null hosts resulted in engraftment of brain parenchyma by bone-marrow-derived myeloid cells of

158 stem cells; and that CVB is carried into the brain parenchyma by developing neurons, which continue t

159 ansporters play a key role in protecting the brain parenchyma by efflux of xenobiotics from capillary

160 xtent than tumor from Tf-CRM107 infused into brain parenchyma by i.v. injection of reagents with low

161 ed viral populations in the meninges and the brain parenchyma by laser capture microdissection.

162 also contributes to the significant loss of brain parenchyma by necrosis that may be reduced by modu

163 ayer of the ventricle and migrate within the brain parenchyma by stimulating an IFN-gamma-dependent d

164 first evidence of gene silencing in injured brain parenchyma by systemically administered siRNA.

165 ese studies suggest that delivery of AraC to brain parenchyma by the IV, IT or IVT routes will be sub

166 nse to brain parenchyma, 2 = hyperintense to brain parenchyma) by a pediatric neuroradiologist who wa

167 of PAR-1 activators, such as thrombin, into brain parenchyma can occur after blood-brain barrier bre

168 antitate the number of SIV-infected cells in brain parenchyma, choroid plexus, and meninges from 17 m

169 ied by increased numbers of parasites in the brain parenchyma compared to infection in wild-type (WT)

170 ress Ang2 were highly invasive into adjacent brain parenchyma compared with isogenic control tumors.

171 en cerebral microvessels and the surrounding brain parenchyma, composed of neuroepithelial cells, gli

172 n expression in the microvasculature and the brain parenchyma contribute to the pathogenesis of AD.

173 lack of professional afferent APCs in naive brain parenchyma contributes to the systemic immune igno

174 iffuse spread of glioma cells throughout the brain parenchyma, contributing to the lethality of GBM.

175 at: (i) transport of fluorescent dextrans in brain parenchyma depended on dextran size in a manner co

176 umbers and that the B lymphocytes within the brain parenchyma display an activated (CD23 positive) ph

177 O2, and pH sensor technology as a monitor of brain parenchyma during and after brain injury, and 2) t

178 When released into the brain parenchyma during hemolysis, Hb becomes a central

179 y of thrombin or other serine proteases into brain parenchyma during intracerebral hemorrhage or extr

180 y lower elasticity and viscosity than normal brain parenchyma, enabling their detection on Gd and Gl

181 0 x 10(-6) mm2/sec) were found within normal brain parenchyma, except in the cortex, where Trace(D) w

182 tic resonance images, whereas the underlying brain parenchyma exhibited minimal involvement.

183 At the end of treatment, tumors, but not brain parenchyma, exhibited extensive infiltration of ac

184 , along which CSF moves into and through the brain parenchyma, facilitating the clearance of intersti

185 gressed, viral protein was identified in the brain parenchyma, first in cells expressing neuron-speci

186 f TP10 exhibits increased penetration of the brain parenchyma following intravenous administration in

187 nezumab can label Abeta that is deposited in brain parenchyma found in sections from Alzheimer's dise

188 nocycline was also capable of protecting the brain parenchyma from necrotic damage as evident by sign

189 that blood vessels sprout passively into the brain parenchyma from pial vascular plexuses to meet met

190 -containing gold nanoparticles can reach the brain parenchyma from systemic administration in mice th

191 permit the AAV.rh10 vector to pass into the brain parenchyma from the vascular system.

192 We found that the brain parenchyma has a functional type I interferon (IFN

193 re to high altitude; however, the CBF of the brain parenchyma has not been studied to date.

194 t to confer neuroprotection by targeting the brain parenchyma has shown promise in experimental strok

195 Patterns of brain parenchyma, hydrocephalus, and so-called middle ce

196 pump, selectively limits drug access to the brain parenchyma, impeding pharmacotherapy of a number o

197 ine blood-brain barrier and was found in the brain parenchyma, implying that it may have antiviral ac

198 that 62% of the (131)I-P-GUS in brain was in brain parenchyma in 2-day-old mice.

199 eraction suppresses accumulation of Abeta in brain parenchyma in a mouse transgenic model.

200 m proteins are known to extravasate into the brain parenchyma in AD due to blood-brain barrier (BBB)

201 demonstrated superior [3H]biotin uptake into brain parenchyma in comparison with the chemical conjuga

202 ts indicate that (131)I-P-GUS transport into brain parenchyma in early postnatal life is mediated by

203 Although fewer CD8+ T cells entered the brain parenchyma in mice depleted of CD4+ T cells, acces

204 migrate from the lateral ventricles into the brain parenchyma in mice.

205 ssure-dependent delivery of 60nm BPNs to the brain parenchyma in regions where the BBB is disrupted b

206 ere are no reports of B lymphocytes entering brain parenchyma in the healthy state.

207 xample of increased endogenous GABA in human brain parenchyma in this disorder.

208 lts evidenced the presence of f-MWNT in mice brain parenchyma, in addition to brain endothelium.

209 due to the effects of pathology outside the brain parenchyma, in particular meningeal inflammation o

210 Diffuse invasion of the brain parenchyma, including along preexisting blood vess

211 However, there was no binding to the brain parenchyma, including the hippocampus, the area wi

212 Coexpression of Flt3L with HA in the brain parenchyma induced a robust systemic anti-HA immun

213 of blood into the subdural space or into the brain parenchyma induced blood volume-dependent increase

214 rgmann glia cells are the first cells of the brain parenchyma infected with LCMV and that the virus s

215 nd brain involvement is rare in IgG4-RD, and brain parenchyma involvement has never been reported.

216 tration of T cells and trypanosomes into the brain parenchyma is a major pathogenetic event in Africa

217 regated amyloid-beta (Abeta) peptides in the brain parenchyma is a pathological hallmark of Alzheimer

218 l nervous system (CNS) relapse involving the brain parenchyma is a rare complication of systemic non-

219 ptibility' in young animals during which the brain parenchyma is at greater risk of acute neutrophil-

220 roper avidity for nanoparticles to reach the brain parenchyma is consistent with recent behavior obse

221 Here, we report that DC migration from brain parenchyma is dependent upon the chemokine recepto

222 After intracerebral hemorrhage (ICH), the brain parenchyma is exposed to blood containing red bloo

223 hanced CT of the head, detection of ischemic brain parenchyma is facilitated by soft-copy review with

224 Although nanoparticle entry into the healthy brain parenchyma is minimal, with no evidence for moveme

225 t of antiretrovirals on virus replication in brain parenchyma is poorly understood.

226 her penetration of MT-II and iodo-MT-II into brain parenchyma is required for the anorectic effect fo

227 At many sites along the borders of the brain parenchyma itself and of the brain blood vessels,

228 kine levels in CSF or serum, rather than the brain parenchyma itself.

229 vely, our results demonstrate that the adult brain parenchyma may recruit and/or generate new neurons

230 ils, small enough to be implanted within the brain parenchyma, may prove to be an effective alternati

231 Despite its tropism for the brain parenchyma, microglial responses to C. koseri have

232 ic gray matter were fronto-parietal areas of brain parenchyma, mostly subependymal region.

233 T cell infiltration and inflammation in the brain parenchyma occurs only when T(H)17 cells outnumber

234 ignal decay curves were biexponential in the brain parenchyma of all volunteers.

235 r constituents of the amyloid plaques in the brain parenchyma of Alzheimer's disease patients.

236 accumulate in the cerebrovascular system and brain parenchyma of diabetic patients.

237 el of the BBB and, most important, enter the brain parenchyma of mice in greater amounts in vivo afte

238 ly inhibited their ability to infiltrate the brain parenchyma of mice.

239 agluc), delivered intravenously and into the brain parenchyma of MPS type VII mice, could provide lon

240 ues in the cerebrocortical blood vessels and brain parenchyma of patients with Alzheimer's disease (A

241 for the first time that oxLDL is present in brain parenchyma of patients with ischemic infarction an

242 ition was also detected in blood vessels and brain parenchyma of patients with late onset AD without

243 ible nitric oxide synthase expression in the brain parenchyma of prion-diseased mice compared with th

244 increased microvascular haemorrhage into the brain parenchyma of Thbs4(KO/KO) mice.

245 ibrillar Abeta deposits were detected in the brain parenchyma or cerebrovasculature.

246 located in leptomeninges (pial vessels) and brain parenchyma (parenchymal vessels) by examining the

247 ecreased to 16 +/- 2 torr (2.1 +/- 0.3 kPa), brain parenchyma PCO2 increased to 105 +/- 44 torr (14 +

248 PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9 kPa); brain parenchyma PCO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa

249 +/- 44 torr (14 +/- 5.9 kPa) (p < .05), and brain parenchyma pH decreased to 6.75 +/- 0.08 (p < .05)

250 On average, brain parenchyma pH gradually returned toward baseline,

251 CO2 of 69 +/- 12 torr (9.2 +/- 1.6 kPa); and brain parenchyma pH of 7.13 +/- 0.09.

252 A biphasic recovery was observed for brain parenchyma pH, which had the slowest recovery of t

253 In six experiments, during the brain insult, brain parenchyma PO2 decreased to 16 +/- 2 torr (2.1 +/-

254 Brain parenchyma PO2 increased from a minimum at the end

255 agreed closely with other published results: brain parenchyma PO2 of 27 +/- 7 (SD) torr (3.6 +/- 0.9

256 after brain injury, and 2) the comparison of brain parenchyma PO2, PCO2, and pH with intracranial pre

257 Monitored variables included brain parenchyma PO2, PCO2, and pH, which were monitored

258 rleukin-1 beta (IL-1 beta) injected into the brain parenchyma produced an intense meningitis and disr

259 GAT2 was not detected in brain parenchyma proper, excluding a role in GABA inacti

260 d features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenes

261 wed that most of the GM-CSF was deposited in brain parenchyma rather than cerebral capillary endothel

262 Virus isolates from the CSF and brain parenchyma readily infected macrophages in culture

263 Necrotic injury in the meninges, but not the brain parenchyma, recruited GFP+ cells within minutes th

264 infiltration of single tumor cells into the brain parenchyma, rendering these deadly tumors virtuall

265 genous cells are able to infiltrate into the brain parenchyma, repositioning themselves into areas pr

266 glioblastoma cells present in non-neoplastic brain parenchyma secrete high levels of TG2 and fibronec

267 In brain parenchyma, serotonin receptors were expressed on

268 MRS of whole-brain parenchyma showed decreases in N-acetylasparate (N

269 The presence of neutrophils within the brain parenchyma significantly contributed to the IL-1be

270 small- and medium-sized vessels deep in the brain parenchyma, such as in the hypothalamus, whereas l

271 d from representative areas of the meninges, brain parenchyma, terminal plasma, and cerebrospinal flu

272 ed through a substantially greater volume of brain parenchyma than mock- and mutant Cx43-transfected

273 ase-resistant PrP fragments (PrP(Sc)) in the brain parenchyma that are infectious to recipient animal

274 d to produce vascular disruptions within rat brain parenchyma that targets single microvessels.

275 sporters is higher in brain barriers than in brain parenchyma; the Cu transport into the brain is mai

276 However, when injected directly into the brain parenchyma, they elicit only transient inflammatio

277 -gp transport topotecan into vCSF and out of brain parenchyma through the blood-brain barrier.

278 of bypassing the BBB and also penetrate the brain parenchyma to achieve a desired effect within the

279 the blood-brain barrier (BBB) and access the brain parenchyma to treat neurological diseases.

280 and the infiltration of neutrophils into the brain parenchyma upon intracranial injection of B. abort

281 In the brain parenchyma, very low constitutive C5aR expression

282 n promoted tumor cell extravasation into the brain parenchyma via permeabilization of the blood-brain

283 , indicating that beta-glucuronidase reached brain parenchyma via the perivascular spaces lining bloo

284 the degree of brain atrophy, the percentage brain parenchyma volume (PBV) relative to that of intrac

285 microbleeds, Virchow-Robin spaces, and total brain parenchyma volume.

286 group than in the control group (P = .007); brain parenchyma volumes were similar.

287 Herniation of meninges and atretic brain parenchyma was also seen through a defect in the o

288 Neutrophil extravasation into the brain parenchyma was impaired in CXCR2 knockout mice and

289 No frank WBCs extravasation in the brain parenchyma was observed.

290 Whereas effector T cells are found in the brain parenchyma where parasites are present, Tregs were

291 reater diffusion of bFGF-HS complex into the brain parenchyma, where it bypassed low-affinity binding

292 cells produce metastatic lesions only in the brain parenchyma, whereas B16 melanoma cells and the som

293 an inherent propensity to invade into normal brain parenchyma, which invariably leads to tumor recurr

294 of therapeutics from the vasculature to the brain parenchyma, which is normally protected by the blo

295 infiltration of single tumor cells into the brain parenchyma, which is thought to involve aberrant i

296 ion and more individual cell infiltration of brain parenchyma with more pronounced perineuronal satel

297 RNA-positive cells scattered throughout the brain parenchyma, with a small number of these cells bei

298 clustered vessels without intervening normal brain parenchyma, with microscopic evidence of hemorrhag

299 que, SIV-infected cells were detected in the brain parenchyma within 7 days of infection.

300 ion of microscopic metastatic lesions in the brain parenchyma, without a decrease in metastasis to th