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1 ood, peripheral tissues, BBB endothelium and brain parenchyma).
2 xchange between the subarachnoid CSF and the brain parenchyma.
3 nt, characterized by diffuse invasion of the brain parenchyma.
4 d an overall complete response in CSF and/or brain parenchyma.
5 eal compartment compared with the underlying brain parenchyma.
6 and flow of cerebrospinal fluid outside the brain parenchyma.
7 ing many small lipophilic molecules from the brain parenchyma.
8 ebral lateral ventricle and infection of the brain parenchyma.
9 and accumulate in a perivascular zone of the brain parenchyma.
10 revents entry of foreign substances into the brain parenchyma.
11 T-cell and trypanosoma infiltration into the brain parenchyma.
12 dothelial cells, whereas 30% were within the brain parenchyma.
13 large reservoir of less soluble Abeta(42) in brain parenchyma.
14 MRL/lpr) lupus mice by IgG infiltration into brain parenchyma.
15 te antigens localized selectively within the brain parenchyma.
16 plaque load, or levels of insoluble Abeta in brain parenchyma.
17 their cognate signaling pathways within the brain parenchyma.
18 stablishment and growth of metastases in the brain parenchyma.
19 tumor growth and invasion of the surrounding brain parenchyma.
20 r determinant of melanoma cell growth in the brain parenchyma.
21 integrity and as such, glioma invasion into brain parenchyma.
22 brain injury, albumin may gain access to the brain parenchyma.
23 , and no HSV antigens were detectable in the brain parenchyma.
24 srupted BBB and diffusely distributed in the brain parenchyma.
25 n brain capillaries than those in the CP and brain parenchyma.
26 n cancer cells while sparing the surrounding brain parenchyma.
27 that 49% of the (131)I-P-GUS in brain was in brain parenchyma.
28 y infiltrate the tumor from the blood or the brain parenchyma.
29 only as diffuse non-fibrillar plaques in the brain parenchyma.
30 tment for isolated CNS relapse involving the brain parenchyma.
31 cur in two locations, namely the pia and the brain parenchyma.
32 vascular conduits and white-matter tracts in brain parenchyma.
33 ivation in situ of bona fide pDCs within the brain parenchyma.
34 ytoid DCs (pDCs; >50-fold; p < 0.001) to the brain parenchyma.
35 nd microglial/macrophage accumulation in the brain parenchyma.
36 crophages and dendritic cells (DCs) into the brain parenchyma.
37 ) facilitates water movement into and out of brain parenchyma.
38 and a transitional zone (Layer IV) into the brain parenchyma.
39 as well as thioflavine S-positive plaques in brain parenchyma.
40 ctively binds to glioma cells but not normal brain parenchyma.
41 etrate brain tumor tissue as well as healthy brain parenchyma.
42 the distribution of the radiolabeled mAb in brain parenchyma.
43 tes perform surveillance functions in normal brain parenchyma.
44 atio of Abeta 40:42 was elevated relative to brain parenchyma.
45 , is lower than in the adjacent, tumour-free brain parenchyma.
46 ammatory responses to dying parasites in the brain parenchyma.
47 ing the peak of T-cell infiltration into the brain parenchyma.
48 in vascular endothelial cells throughout the brain parenchyma.
49 ated by the accumulation of serum IgG in the brain parenchyma.
50 e for the presence of this connexin in adult brain parenchyma.
51 hat inhibit the accumulation of Abeta in the brain parenchyma.
52 h occasional members interspersed throughout brain parenchyma.
53 h microglia and astrocytes in plaques in the brain parenchyma.
54 ancer cell adhesion and trafficking into the brain parenchyma.
55 ocytes and a population of astrocytes in the brain parenchyma.
56 the brain and meninges, and extends into the brain parenchyma.
57 It is converted in AD to a fibrillar form in brain parenchyma.
58 d encephalitis that extended deeply into the brain parenchyma.
59 allowing the entry of these agents into the brain parenchyma.
60 HOS and passed into the CSF but not into the brain parenchyma.
61 e exacerbated by the buildup of Abeta in the brain parenchyma.
62 Microglia dynamically survey the brain parenchyma.
63 mechanism of convective solute transport in brain parenchyma.
64 but was essential for trafficking within the brain parenchyma.
65 brain, leading to a mass of blood within the brain parenchyma.
66 cellular transport between the blood and the brain parenchyma.
67 particle localisation is observed within the brain parenchyma.
68 ctivity on magnetic resonance imaging in the brain parenchyma.
69 nels facilitate convective transport through brain parenchyma.
70 emigrate preferentially into ischemic cortex brain parenchyma.
71 vasculature to migrate within the developing brain parenchyma.
72 rowth by metastatic lung cancer cells in the brain parenchyma.
73 the detectable tumor and in the surrounding brain parenchyma.
74 he case of capillaries) immediately adjacent brain parenchyma.
75 are being developed to remove Abeta from the brain parenchyma.
76 s presented as remarkably softer than normal brain parenchyma.
77 ystemically circulated tracer leaks into the brain parenchyma.
78 hree-point ordinal scale (0 = hypointense to brain parenchyma, 1 = isointense to brain parenchyma, 2
79 tense to brain parenchyma, 1 = isointense to brain parenchyma, 2 = hyperintense to brain parenchyma)
81 generally infiltrate the surrounding normal brain parenchyma, a process associated with increased va
82 lenge in the TMEV model is directly into the brain parenchyma, a site that is considered immune privi
83 o extracellular beta-amyloid deposits in the brain parenchyma (Abeta plaques) and in the vasculature
84 iffers substantially from humans because the brain parenchyma accumulates numerous, diffuse, nonfibri
85 cular organs and disseminated throughout the brain parenchyma, accumulating on the plasma membranes o
86 We next demonstrated peptide delivery to the brain parenchyma after in vivo delivery by detecting bio
88 e finding that rh Bri2 BRICHOS can reach the brain parenchyma after peripheral administration may be
91 the tight extracellular migration tracts in brain parenchyma, allowed high-content time-resolved ima
92 ary structure and labels amyloid in both the brain parenchyma (amyloid plaques) and blood vessels.
93 tein (Abeta) fibrils into plaques within the brain parenchyma and along cerebral blood vessels is a h
94 beta might lead to amyloid deposition in the brain parenchyma and blood vessel walls, potentially res
95 lele, Abeta was effectively cleared from the brain parenchyma and brain microglial activation was red
97 of studied radiolabelled f-MWNT in the whole brain parenchyma and capillaries while 3D-single photon
98 is the deposition of amyloid beta (Abeta) in brain parenchyma and cerebral blood vessels, accompanied
103 ition of the Abeta peptides deposited in the brain parenchyma and cerebrovascular walls of triple tra
105 calization of klotho mRNA and protein in rat brain parenchyma and demonstrate that klotho levels vary
106 have a distinctive ability to infiltrate the brain parenchyma and disrupt the neural extracellular ma
107 ce astroglial scarring at boundaries between brain parenchyma and fluids, and at junctions between gr
108 inear discriminant model used to distinguish brain parenchyma and gliomas yielded an overall sensitiv
110 of cerebrospinal fluid CD4 T cells into the brain parenchyma and highlight implications on brain imm
111 hemoglobin delocalization from CSF into the brain parenchyma and into the NO-sensitive compartment o
112 eposition of beta-amyloid (Abeta) within the brain parenchyma and its subsequent accumulation into se
113 43 are the main Abeta peptides deposited in brain parenchyma and LMD-CWPs in association with the PS
114 letal level, which enables it to protect the brain parenchyma and maintain a homeostatic environment.
116 s yet unclear whether and how they enter the brain parenchyma and migrate to target specific Ags.
117 ogist's review of the imaging studies of the brain parenchyma and of the degree of carotid stenosis,
118 lecules (PBAE-PEG) rapidly penetrate healthy brain parenchyma and orthotopic brain tumor tissues in r
119 were found in increased numbers in both the brain parenchyma and perivascular spaces of pre-AIDS bra
122 pillaries with subsequent transport into the brain parenchyma and specific uptake into TfR1-positive
123 eripheral cytokine interleukin-6 (IL-6) into brain parenchyma and subsequent expression of depression
125 e levels of virus were also found within the brain parenchyma and the cerebrospinal fluid (CSF), with
126 cts of long term implantation on surrounding brain parenchyma and the resulting alterations in the fu
127 erapeutic polypeptides from the blood to the brain parenchyma and thus hinders effective treatment of
128 IA binding phenotype, effectively enters the brain parenchyma and transduces neurons at levels compar
129 es of individual beta-amyloid plaques in the brain parenchyma and vasculature and requires no stainin
130 showed increased superoxide formation in the brain parenchyma and vasculature during reperfusion.
132 pal component of amyloid deposits within the brain parenchyma, and an increase in the Abeta42/Abeta40
133 ed in increases in mAb (P < 0.05) in plasma, brain parenchyma, and cerebrospinal fluid and decreases
134 vary on where klotho is expressed within the brain parenchyma, and no data is available as to whether
135 r (BBB) provides limited immune privilege to brain parenchyma, and the immune response to recombinant
136 or cells disperse extensively throughout the brain parenchyma, and the need for tumor-specific drug t
137 s of both 45 nm and 80 nm diameter reach the brain parenchyma, and their accumulation there (visualiz
138 hly ramified processes constantly survey the brain parenchyma, and they respond promptly to brain dam
139 sponse, namely, professional APCs within the brain parenchyma, and this could counteract the intrinsi
140 virus, which was directly injected into the brain parenchyma, and to determine whether this response
141 ) and beta-amyloid (Abeta) deposition in the brain parenchyma are hallmarks of Alzheimer's disease (A
143 cause prolonged increases in 2-AG amounts in brain parenchyma are thought to orchestrate neuroinflamm
144 Microglia, the resident macrophages of the brain parenchyma, are key players in central nervous sys
145 patients with isolated CNS relapse with the brain parenchyma as initial relapse site were eligible.
146 y amyloid-beta (Abeta) peptide deposition in brain parenchyma as plaques and in cerebral blood vessel
149 e widespread distribution of therapeutics in brain parenchyma away from the point of local administra
151 y conventional radiological modalities, i.e. brain parenchyma, bones and extremities, can be evaluate
152 tis and perivascular cuffing not only in the brain parenchyma but also in the spinal cord, with no ev
153 marked decrease in plaque deposition in the brain parenchyma but an equally striking increase in CAA
154 ells significantly reduced metastasis to the brain parenchyma but did not induce metastasis to the le
155 2 reduction decreased amyloid plaques in the brain parenchyma but promoted the development of cerebro
157 h quantifies biomechanical properties of the brain parenchyma by analyzing the propagation of externa
158 Mecp2-null hosts resulted in engraftment of brain parenchyma by bone-marrow-derived myeloid cells of
159 stem cells; and that CVB is carried into the brain parenchyma by developing neurons, which continue t
160 ansporters play a key role in protecting the brain parenchyma by efflux of xenobiotics from capillary
161 xtent than tumor from Tf-CRM107 infused into brain parenchyma by i.v. injection of reagents with low
163 also contributes to the significant loss of brain parenchyma by necrosis that may be reduced by modu
164 ayer of the ventricle and migrate within the brain parenchyma by stimulating an IFN-gamma-dependent d
165 first evidence of gene silencing in injured brain parenchyma by systemically administered siRNA.
166 ese studies suggest that delivery of AraC to brain parenchyma by the IV, IT or IVT routes will be sub
167 nse to brain parenchyma, 2 = hyperintense to brain parenchyma) by a pediatric neuroradiologist who wa
168 of PAR-1 activators, such as thrombin, into brain parenchyma can occur after blood-brain barrier bre
169 umor necrosis factor alpha (TNFalpha) in the brain parenchyma causes cerebral overexpression of Inter
170 antitate the number of SIV-infected cells in brain parenchyma, choroid plexus, and meninges from 17 m
171 ied by increased numbers of parasites in the brain parenchyma compared to infection in wild-type (WT)
172 ress Ang2 were highly invasive into adjacent brain parenchyma compared with isogenic control tumors.
173 en cerebral microvessels and the surrounding brain parenchyma, composed of neuroepithelial cells, gli
174 lack of professional afferent APCs in naive brain parenchyma contributes to the systemic immune igno
175 iffuse spread of glioma cells throughout the brain parenchyma, contributing to the lethality of GBM.
176 at: (i) transport of fluorescent dextrans in brain parenchyma depended on dextran size in a manner co
177 umbers and that the B lymphocytes within the brain parenchyma display an activated (CD23 positive) ph
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
182 At the end of treatment, tumors, but not brain parenchyma, exhibited extensive infiltration of ac
183 , along which CSF moves into and through the brain parenchyma, facilitating the clearance of intersti
184 gressed, viral protein was identified in the brain parenchyma, first in cells expressing neuron-speci
185 f TP10 exhibits increased penetration of the brain parenchyma following intravenous administration in
186 nezumab can label Abeta that is deposited in brain parenchyma found in sections from Alzheimer's dise
187 nocycline was also capable of protecting the brain parenchyma from necrotic damage as evident by sign
188 that blood vessels sprout passively into the brain parenchyma from pial vascular plexuses to meet met
189 -containing gold nanoparticles can reach the brain parenchyma from systemic administration in mice th
193 t to confer neuroprotection by targeting the brain parenchyma has shown promise in experimental strok
195 pump, selectively limits drug access to the brain parenchyma, impeding pharmacotherapy of a number o
196 ine blood-brain barrier and was found in the brain parenchyma, implying that it may have antiviral ac
197 a structural determinant of MHV entry in the brain parenchyma important for altered neuropathogenesis
200 m proteins are known to extravasate into the brain parenchyma in AD due to blood-brain barrier (BBB)
201 owed excellent contrast with the surrounding brain parenchyma in all patients with active disease.
202 ts indicate that (131)I-P-GUS transport into brain parenchyma in early postnatal life is mediated by
204 s were identified by immunohistochemistry in brain parenchyma in over 40% of "high inflammation" schi
205 ssure-dependent delivery of 60nm BPNs to the brain parenchyma in regions where the BBB is disrupted b
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 usions contact different neural cells in the brain parenchyma including blood vessels and neurons, an
214 rgmann glia cells are the first cells of the brain parenchyma infected with LCMV and that the virus s
215 Microglial processes continuously survey the brain parenchyma, interact with synaptic elements and ma
216 nd brain involvement is rare in IgG4-RD, and brain parenchyma involvement has never been reported.
217 loid beta (Abeta) plaques and fibrils in the brain parenchyma is a hallmark of Alzheimer's disease (A
218 tration of T cells and trypanosomes into the brain parenchyma is a major pathogenetic event in Africa
219 regated amyloid-beta (Abeta) peptides in the brain parenchyma is a pathological hallmark of Alzheimer
220 l nervous system (CNS) relapse involving the brain parenchyma is a rare complication of systemic non-
221 roper avidity for nanoparticles to reach the brain parenchyma is consistent with recent behavior obse
223 After intracerebral hemorrhage (ICH), the brain parenchyma is exposed to blood containing red bloo
224 hanced CT of the head, detection of ischemic brain parenchyma is facilitated by soft-copy review with
225 Although nanoparticle entry into the healthy brain parenchyma is minimal, with no evidence for moveme
228 her penetration of MT-II and iodo-MT-II into brain parenchyma is required for the anorectic effect fo
229 c transport, including solute clearance from brain parenchyma, is impaired during evolving hypertensi
232 virus [IAV]) remains detectable in the mouse brain parenchyma long after resolution of the acute infe
233 tion of human glioma cells (hGCs) within the brain parenchyma makes glioblastoma one of the most aggr
234 vely, our results demonstrate that the adult brain parenchyma may recruit and/or generate new neurons
235 ils, small enough to be implanted within the brain parenchyma, may prove to be an effective alternati
238 lecule entities capable of crossing into the brain parenchyma, novel formulations of existing chemoth
239 T cell infiltration and inflammation in the brain parenchyma occurs only when T(H)17 cells outnumber
240 alitis is a condition of inflammation of the brain parenchyma, occurs as a result of infectious or au
244 nique pathological bulbar vacuolation in the brain parenchyma of infected mice with persistent CD11b(
245 el of the BBB and, most important, enter the brain parenchyma of mice in greater amounts in vivo afte
247 ues in the cerebrocortical blood vessels and brain parenchyma of patients with Alzheimer's disease (A
248 for the first time that oxLDL is present in brain parenchyma of patients with ischemic infarction an
249 ition was also detected in blood vessels and brain parenchyma of patients with late onset AD without
251 ible nitric oxide synthase expression in the brain parenchyma of prion-diseased mice compared with th
252 led that TNAP activity was suppressed in the brain parenchyma of SBI-425-treated mice compared to con
255 ydrogel can release cancer therapeutics into brain parenchyma over a long period of time, suppressing
256 located in leptomeninges (pial vessels) and brain parenchyma (parenchymal vessels) by examining the
259 d features of extensive invasion into normal brain parenchyma, rapid growth, necrosis, and angiogenes
261 Necrotic injury in the meninges, but not the brain parenchyma, recruited GFP+ cells within minutes th
262 infiltration of single tumor cells into the brain parenchyma, rendering these deadly tumors virtuall
263 genous cells are able to infiltrate into the brain parenchyma, repositioning themselves into areas pr
264 glioblastoma cells present in non-neoplastic brain parenchyma secrete high levels of TG2 and fibronec
268 small- and medium-sized vessels deep in the brain parenchyma, such as in the hypothalamus, whereas l
269 d from representative areas of the meninges, brain parenchyma, terminal plasma, and cerebrospinal flu
270 ed through a substantially greater volume of brain parenchyma than mock- and mutant Cx43-transfected
271 ase-resistant PrP fragments (PrP(Sc)) in the brain parenchyma that are infectious to recipient animal
274 sporters is higher in brain barriers than in brain parenchyma; the Cu transport into the brain is mai
275 However, when injected directly into the brain parenchyma, they elicit only transient inflammatio
277 of bypassing the BBB and also penetrate the brain parenchyma to achieve a desired effect within the
278 transported from the subarachnoid space into brain parenchyma to exchange with interstitial fluid (al
280 and the infiltration of neutrophils into the brain parenchyma upon intracranial injection of B. abort
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
290 etween ventricles and different parts of the brain parenchyma were revealed suggesting a possible rol
291 Whereas effector T cells are found in the brain parenchyma where parasites are present, Tregs were
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 events most drugs from gaining access to the brain parenchyma, which is a recognized impediment to th
295 of therapeutics from the vasculature to the brain parenchyma, which is normally protected by the blo
296 infiltration of single tumor cells into the brain parenchyma, which is thought to involve aberrant i
297 more subtle pathological alterations of the brain parenchyma, which may eventually lead to neurologi
298 plasma proteins readily permeate the healthy brain parenchyma, with transport maintained by BBB-speci
299 ssed the blood-brain-barrier and entered the brain parenchyma within 2 minutes of being in the blood.
300 ion of microscopic metastatic lesions in the brain parenchyma, without a decrease in metastasis to th