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1 BBB disruption, evaluated by mapping the R1 relaxation r
2 BBB dysfunction, however, is evident in many neurologica
3 BBB-impermeable fluorescent tracer injected transcardial
6 a partial conversion of non-BBB CNS ECs to a BBB-like state, has little or no effect on gene expressi
7 in targeting, including drug delivery across BBB and direct nose-to-brain drug delivery along with th
10 ficacy in GBM, in vitro 3D models of GBM and BBB leveraging patient- or healthy-individual-derived ce
12 an overview of current 3D-bioprinted GBM and BBB models is provided, elaborating on the microenvironm
13 e microenvironmental compositions of GBM and BBB, relevant biomaterials to mimic the native tissues,
16 monstrates the distinct cellular uptakes and BBB penetrations through receptor-mediated transcytosis.
17 althy rats confirmed that both compounds are BBB permeable and that bladder accumulation is low until
20 (13)C-AcAc to cross the blood brain barrier (BBB) and its potential to monitor brain metabolism remai
22 into the brain, causing blood-brain barrier (BBB) breakdown, extravasation of autoantibodies into the
23 92) or without (n = 90) blood-brain barrier (BBB) disruption and a diseased control group with cluste
24 hase (NOS) in mediating blood-brain barrier (BBB) disruption and peripheral immune cell infiltration
25 investigated controlled blood-brain barrier (BBB) disruption using a low-frequency clinical transcran
27 is often implicated in blood-brain barrier (BBB) dysfunction, but whether and how GLUT1 controls EC
28 llowing TBI, leading to blood brain barrier (BBB) dysfunction, neuronal damage and long term neuronal
29 f Abeta42 and cross the blood-brain barrier (BBB) following intravenous administration without notice
30 hy (CAA), which impairs blood-brain barrier (BBB) function and accelerates cognitive degeneration.
31 nt of robust assays for blood-brain barrier (BBB) function, including drug permeability and extrusion
34 n important role at the blood-brain barrier (BBB) in promoting clearance of neurotoxic beta-amyloid (
35 ic social stress alters blood-brain barrier (BBB) integrity through loss of tight junction protein cl
36 ers of inflammation and blood-brain barrier (BBB) integrity were measured preoperatively and up to 48
40 d that breakdown of the blood-brain barrier (BBB) is an early biomarker of human cognitive dysfunctio
47 em cell (hiPSC)-derived blood-brain barrier (BBB) models established to date lack expression of key a
48 NS) induces endothelial blood-brain barrier (BBB) opening as well as the formation of a tight junctio
57 Transfer across the blood-brain barrier (BBB) remains a significant hurdle for the development of
58 rug delivery across the blood-brain barrier (BBB) remains a significant obstacle for the development
61 iological barriers, the blood-brain barrier (BBB) strongly impede hurdle for drug transport to brain.
62 ls contain a functional blood-brain barrier (BBB) that is necessary for neuronal survival and activit
63 impenetrability of the blood-brain barrier (BBB) to most conventional drugs impedes the treatment of
64 enters by crossing the blood-brain barrier (BBB) via macrophages, which are considered as conduits b
65 ogic restoration of the blood-brain barrier (BBB), 12 mo after murine TBI, is associated with arreste
66 cular components of the blood-brain barrier (BBB), a specialized neurovascular unit evolved to mainta
67 es the integrity of the blood-brain barrier (BBB), and infects the CNS in the early stages of infecti
68 d a functionally intact blood-brain barrier (BBB), and so are shielded from exposure to therapeutic d
69 gliosis, erosion of the blood-brain barrier (BBB), formation of inflammatory cytokines, and brain inf
71 the brain, known as the blood-brain barrier (BBB), is understood to maintain brain function in part v
72 capable of crossing the blood-brain barrier (BBB), thereby enabling the delivery of therapeutic genes
73 munotherapy through the blood-brain barrier (BBB), together with the brain's unique biochemical and a
74 eability changes in the blood brain barrier (BBB), which may eventually result in the pathogenesis of
75 transiently disrupt the blood-brain barrier (BBB), which may induce a sterile inflammation response.
76 properties, termed the blood-brain barrier (BBB), which stringently regulate the entry of molecules
93 er (L-NAME) administered after blast blocked BBB disruption and prevented CD4(+) T-cell infiltration
94 nables the chemotherapeutic to overcome both BBB and multidrug resistance (MDR) glioma cells while pr
95 -retina barrier and blood-brain barrier (BRB/BBB) are selective and semipermeable and are critical fo
96 e strategy for the development of better BRB/BBB models and novel EC barrier-inducing therapeutics.
103 hese results demonstrate safe and controlled BBB disruption with a low-frequency clinical TcMRgFUS de
104 in transient hypervascularization but delays BBB maturation in specific CNS regions, as evidenced by
105 gether, we introduce the first hiPSC-derived BBB model that displays an adhesion molecule phenotype t
106 ug delivery, how multiple cell types dictate BBB function and the role of the BTB in disease progress
110 crucial extracellular matrix protein during BBB maturation that regulates cell-cell interactions and
111 osome/lysosome pathway (with high-efficiency BBB crossing observed in vitro), while competing for the
112 ess, altered expression of genes crucial for BBB barrier functioning nor reduced vascular function.
113 Wnt/beta-catenin signaling is essential for BBB development, its downstream targets within the neuro
115 processes can be used to safely advance FUS-BBB opening into a wider range of clinical applications.
117 ledge of the secondary effects caused by FUS-BBB opening on brain physiology, identify areas that rem
118 information would help to safely expand FUS-BBB opening protocols into a wider range of drug deliver
120 ndary effects is becoming vital now that FUS-BBB opening treatments have entered clinical trials.
122 the key structure and function of the human BBB and enables 3D mapping of nanoparticle distributions
125 stems which have potential to cross impaired BBB, target and deliver drugs selectively to activated m
126 EVG nanoformulation demonstrated an improved BBB model penetration cross the in vitro BBB model and a
127 was more effective (P < 0.05) for improving BBB permeation and brain accumulation of the darunavir p
130 injected exogenous tracers-as is standard in BBB studies-fully represents blood-to-brain transport.
131 d biopsy (FUS-LBx) that uses FUS to increase BBB permeability in murine glioblastoma models and thus
141 antially lower in invasive tumor rim (intact BBB) compared to glioblastoma core (disrupted BBB).
143 f other forms of neurodegeneration involving BBB deterioration (e.g., Alzheimer's disease, Parkinson'
146 olecular mechanisms of miR-15a/16-1-mediated BBB dysfunction may enable the discovery of new therapie
147 linical trials investigating MRgFUS-mediated BBB opening, which may ameliorate DIPG chemotherapeutic
149 ll (iPSC)-derived BMEC-like cells as a model BBB substrate on which to mine for new RMT-targeting ant
153 in vivo leads to a partial conversion of non-BBB CNS ECs to a BBB-like state, has little or no effect
154 ) and delivers neurotensin, an otherwise non-BBB-penetrant neuropeptide, at levels capable of modulat
155 of P7C3-A20, including restoration of normal BBB endothelium length, increased brain capillary pericy
156 niques, and the development of biomarkers of BBB integrity along with systems biology approaches, sho
158 anoid model recapitulates characteristics of BBB dysfunction under hypoxic physiological conditions a
160 residues, S269 and N472, as determinants of BBB crossing for AAVrh.10 and AAVrh.39, a feature utiliz
161 eolin-1 (cav-1) are critical determinants of BBB integrity that can regulate barrier properties of th
163 ry pericyte density, increased expression of BBB tight junction proteins, reduced brain infiltration
165 ssociated with a rapid and selective loss of BBB transcripts and chromatin features, as well as a gre
166 m albumin levels in the cortex, a measure of BBB breakdown, were significantly higher after SE in EP2
169 duced cell death, as well as preservation of BBB integrity in mice after exposure to toxic levels of
172 he safety, feasibility, and reversibility of BBB opening with FUS treatment of the hippocampus and en
176 single blast exposure, induced delayed-onset BBB disruption (72 hours post-blast) in cerebellum.
179 ent was clearly depicted in those with overt BBB disruption, while paravenous and parasinus meningeal
182 , mice lacking Th17 lymphocytes have reduced BBB leakage, microglial activation, and antibody infiltr
183 15a/16-1 had smaller brain infarcts, reduced BBB leakage, and decreased infiltration of peripheral im
184 y, knockout of miR-34a significantly reduces BBB permeability, alleviates disruption of tight junctio
186 In particular, neuronal activity regulates BBB efflux transporter expression and function, which is
187 on in brain endothelial cells that regulates BBB permeability in inflammatory conditions.SIGNIFICANCE
190 le destabilization occurred resulted in safe BBB openings, as shown by MR images and gross pathology.
193 articles (STICK-NPs) can sequentially target BBB/BBTB and brain tumor cells with surface maltobionic
194 iously reported the feasibility of temporary BBB opening within the normal murine brainstem using MRg
197 rategies to improve drug delivery across the BBB and BTB and discuss their impact on improving conven
198 imate the rate of virus transport across the BBB as well as viral replication inside the brain, and w
201 nm; hydrodynamic diameter 3-4 nm) across the BBB was studied as a function of time by confocal laser
203 ration of metastatic cancer cells across the BBB, offering new targets for the development of gene an
208 -GBM co-culture model was used to assess the BBB permeability and anti-tumor activity of the DOX-EDT-
209 lopramide can measure ABCB1 induction at the BBB in a beta-amyloidosis mouse model (APP/PS1-21 mice)
212 H expression within endothelial cells at the BBB, then demonstrated that DHH is down-regulated during
215 eriphery, the protection of the brain by the BBB offers an isolated sanctuary to harbor HIV and maint
217 n-mimetic nanoparticles (eHNPs) to cross the BBB and deliver a SHH inhibitor effectively to the cance
218 et need for drug carriers that can cross the BBB and deliver drugs to targeted sites with high drug-l
222 proteins and viral particulates to cross the BBB, we engineered a synthetic protein nanoparticle (SPN
223 AR antibody to TfR1 that rapidly crosses the BBB and exhibits a favorable pharmacokinetic and safety
225 ocyte-derived macrophages after crossing the BBB model without altering the BBB model integrity.
228 pressed in surface glial cells that form the BBB, and EcI knockdown in the BBB suppresses ecdysone si
229 ed on cerebral endothelial cells forming the BBB, regulate immune cell infiltration across this barri
230 ids underwent hypoxia (0.1% O(2); 24 h), the BBB was more permeable, permitting the uptake of more na
231 that form the BBB, and EcI knockdown in the BBB suppresses ecdysone signaling within the CNS and blo
232 culture system, the CNS requires EcI in the BBB to incorporate ecdysone from the culture medium.
235 1-14), leads to accelerated breakdown of the BBB and degeneration of brain capillary pericytes(15-19)
237 gical diseases owing to the existence of the BBB and the blood-spinal cord barrier have been terrible
238 novel mechanisms underlying crossing of the BBB by (D)CDX-modified liposomes, suggesting that (D)CDX
239 y diffuse through the plasma membrane of the BBB cells to reach the brain [1], because of the predomi
240 Our findings suggest that breakdown of the BBB contributes to APOE4-associated cognitive decline in
242 is based on a time-dependent opening of the BBB for nanoparticles, followed by a rapid diffusion int
248 The development of an in-vitro mimic of the BBB requires recapitulating the correct phenotype of the
250 cessing occurs within the endothelium of the BBB, but any influence on transcytosis remains unclear.
251 is review, we elucidate the pathology of the BBB, its ability to potentiate viral replication, as wel
253 are known to compromise the integrity of the BBB, resulting in a vasculature known as the blood-tumou
254 re correlated with increased activity of the BBB-degrading cyclophilin A-matrix metalloproteinase-9 p
255 model demonstrated the effectiveness of the BBB-penetrating combination therapy and the macrophage-m
256 M-1) and a decrease in the expression of the BBB-related tight junction protein, Zonula occludens-1 (
261 sed ultrasound (FUS) can reversibly open the BBB and facilitate delivery of targeted brain therapeuti
263 binding peptide for transiently opening the BBB tight junctions are expected to enhance the efficacy
265 we found that endothelial Dhh both opens the BBB via the modulation of forkhead box O1 (FoxO1) transc
269 -derived Sonic hedgehog (SHH) stabilizes the BBB during CNS inflammatory disease, while endothelial-d
272 hibiting penetration of the drug through the BBB and is a valid targeting strategy for drugs to facil
274 n of how ecdysone enters the CNS through the BBB to exert its diverse role in Drosophila brain develo
275 bidirectional transport of BDNF through the BBB, we tested the hypothesis that plasma BDNF may be us
276 the dynamics of monocyte recruitment to the BBB and the highly regionalized localization of monocyte
277 ing increased opportunities to transpass the BBB/BBTB via glucose-transporter-mediated transcytosis b
279 ch this can be performed safely, whereby the BBB is disrupted to the point of being permeable to norm
281 identify active molecular changes within the BBB associated with stress resilience that might serve a
285 ets of Wnt/beta-catenin signaling underlying BBB maturation, we performed a microarray analysis that
289 ved BBB model penetration cross the in vitro BBB model and an enhanced HIV-1 suppression in HIV-1-inf
290 is EVG nanoformulation to cross the in vitro BBB model and suppress the HIV-1 in macrophage cells.
292 s associated liposomes) to cross an in vitro BBB using a simulated cerebral endothelium monolayer for
296 hronic neuroinflammatory tolerance" in which BBB opening in the resting state is sufficient to stimul
297 the healthy brain, a mechanism of widespread BBB dysfunction with age and a strategy for enhanced dru
298 n were significantly higher (P < 0.001) with BBB disruption, but SN-38 was only detected in <50% of t
299 Strikingly, this does not coincide with BBB leakiness, altered expression of genes crucial for B