Evaluation of blood–brain barrier-stealth nanocomposites for in situ glioblastoma theranostics applications

Nanoscale ◽  
2016 ◽  
Vol 8 (15) ◽  
pp. 7866-7870 ◽  
Author(s):  
Chia-Hao Su ◽  
Ching-Yi Tsai ◽  
Boguslaw Tomanek ◽  
Wei-Yu Chen ◽  
Fong-Yu Cheng
Keyword(s):  
Animal Model ◽  
Antitumor Activity ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

A novel BBB-stealth nanocomposite show the antitumor activity in in vivo and in situ glioblastoma animal model, MRI, and IVIS® Spectrum.

Interactions of IGF-1 with the Blood-Brain Barrier in vivo and in situ

2000 ◽  
Vol 72 (3) ◽  
pp. 171-178 ◽  
Author(s):  
Weihong Pan ◽  
Abba J. Kastin
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Blood Brain

scholarly journals Clonidine Transport at the Mouse Blood—Brain Barrier by a New H+ Antiporter that Interacts with Addictive Drugs

2009 ◽  
Vol 29 (7) ◽  
pp. 1293-1304 ◽  
Author(s):  
Pascal André ◽  
Marcel Debray ◽  
Jean-Michel Scherrmann ◽  
Salvatore Cisternino
Keyword(s):  
Blood Brain Barrier ◽  
Brain Perfusion ◽  
Brain Parenchyma ◽  
Brain Barrier ◽  
Blood Brain ◽  
Cationic Compounds ◽  
Cns Drugs ◽  
The Brain

Identifying drug transporters and their in vivo significance will help to explain why some central nervous system (CNS) drugs cross the blood-brain barrier (BBB) and reach the brain parenchyma. We characterized the transport of the drug Clonidine at the luminal BBB by in situ mouse brain perfusion. Clonidine influx was saturable, followed by Michaelis–Menten kinetics ( Km = 0.62 mmol/L, Vmax = 1.76 nmol/sec per g at pH 7.40), and was insensitive to both sodium and trans-membrane potential. In vivo manipulation of intracellular and/or extracellular pH and Trans-stimulation showed that Clonidine was transported by an H+-coupled antiporter regulated by both proton and Clonidine gradients, and that diphenhydramine was also a substrate. Organic cation transporters (Oct1–3), P-gp, and Bcrp did not alter Clonidine transport at the BBB in knockout mice. Secondary or tertiary amine CNS compounds such as oxycodone, morphine, diacetylmorphine, methylenedioxyamphetamine (MDMA), cocaine, and nicotine inhibited Clonidine transport. However, cationic compounds that interact with choline, Mate, Octn, and Pmat transporters did not. This suggests that Clonidine is transported at the luminal mouse BBB by a new H+-coupled reversible antiporter.

Hyperosmolar blood-brain barrier disruption in baboons: an in vivo study using positron emission tomography and rubidium-82

1996 ◽  
Vol 84 (3) ◽  
pp. 494-502 ◽  
Author(s):  
Bernhard Zünkeler ◽  
Richard E. Carson ◽  
Jeffrey Olson ◽  
Ronald G. Blasberg ◽  
Mary Girton ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Brain Tumors ◽  
Blood Brain Barrier ◽  
Emission Tomography ◽  
Brain Barrier ◽  
Blood Brain ◽  
Positron Emission ◽  
The Mean ◽  
Rubidium 82

✓ Hyperosmolar blood-brain barrier (BBB) disruption remains controversial as an adjuvant therapy to increase delivery of water-soluble compounds to extracellular space in the brain in patients with malignant brain tumors. To understand the physiological effects of BBB disruption more clearly, the authors used positron emission tomography (PET) to study the time course of BBB permeability in response to the potassium analog rubidium-82 (82Rb, halflife 75 seconds) following BBB disruption in anesthetized adult baboons. Mannitol (25%) was injected into the carotid artery and PET scans were performed before and serially at 8- to 15-minute intervals after BBB disruption. The mean influx constant (K1), a measure of permeability-surface area product, in ipsilateral, mannitol-perfused mixed gray- and white-matter brain regions was 4.9 ± 2.4 µl/min/ml (± standard deviation) at baseline and increased more than 100% (ΔK1 = 9.4 ± 5.1 µl/min/ml, 18 baboons) in brain perfused by mannitol. The effect of BBB disruption on K1 correlated directly with the total amount of mannitol administered (p < 0.005). Vascular permeability returned to baseline with a halftime of 24.0 ± 14.3 minutes. The mean brain plasma volume rose by 0.57 ± 0.34 ml/100 ml in ipsilateral perfused brain following BBB disruption. This work provides a basis for the in vivo study of permeability changes induced by BBB disruption in human brain and brain tumors.

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