We hypothesized that custom-designed microemulsions would effectively scavenge compounds from bulk media. Pluronic-based oil-in-water microemulsions were synthesized that efficiently reduced the free concentration of the local anesthetic bupivacaine in 0.9% NaCl. Both the molecular nature and concentration of the constituents in the microemulsions significantly affected extraction efficiencies. Pluronic F127-based microemulsions extracted bupivacaine more efficiently than microemulsions synthesized using other Pluronic surfactants (L44, L62, L64, F77, F87, F88, P104). Extraction was markedly increased by addition of fatty acid sodium salts due to greater oil/water interface area, increased columbic interaction between bupivacaine and fatty acids sodium salt, and greater surface activity. These data suggest that oil-in-water microemulsions may be an effective agent to treat cardiotoxicity caused by bupivacaine or other lipophilic drugs.

ZnO nanorod-gated AlGaN∕GaN high electron mobility transistors (HEMTs) are demonstrated for the detection of glucose. A ZnO nanorod array was selectively grown on the gate area using low temperature hydrothermal decomposition to immobilize glucose oxidase (GOx). The one-dimensional ZnO nanorods provide a large effective surface area with high surface-to-volume ratio and provide a favorable environment for the immobilization of GOx. The AlGaN∕GaN HEMT drain-source current showed a rapid response of less than 5s when target glucose in a buffer with a pH value of 7.4 was added to the GOx immobilized on the ZnO nanorod surface. We could detect a wide range of concentrations from 0.5nMto125μM. The sensor exhibited a linear range from 0.5nMto14.5μM and an experiment limit of detection of 0.5nM. This demonstrates the possibility of using AlGaN∕GaN HEMTs for noninvasive exhaled breath condensate based glucose detection of diabetic application.

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Oil-filled nanocapsules were synthesized using the oil droplets of an O/W microemulsion as templates. A polysiloxane/silicate shell was formed at the surface of the oil droplet by cross-linking n-octadecyltrimethoxysilane and tetramethoxysiloxane. The shell imparted stability to the oil droplets against coalescence. The nanocapsules can be used in a number of applications (i.e., biomedical or environmental) where the free concentration of lipophilic compounds must be reduced. As a proof, the nanocapsules (1.4% w/v oil content in saline) were shown to sequester quinoline (8 μM) from saline in <15 min. The removal process was followed in real time using the UV absorbance of free quinoline in solution. Our primary goal is to produce a system for drug detoxification therapy. As a proof of concept for sequestering drugs, the nanocapsules were used in the removal of free bupivacaine from normal saline solution. The free bupivacaine concentration was determined in the aqueous phase after contact with such nanocapsules using HPLC. The results showed a rapid removal of bupivacaine. The nanocapsules at a concentration of 0.1% w/v oil content showed a maximum removal capacity of ≈1900 μM bupivacaine.

Adenosine activates adenosine-induced inwardly rectifying K+ current (IKAdo) and inhibits isoproterenol (100 nM)-stimulated L-type Ca2+ current (beta-ICa,L) of guinea pig atrial myocytes with EC50 values of 2.17 and 0.20 microM, respectively. We determined whether this 11-fold difference in potency of adenosine is due to the existence of a greater A1 adenosine receptor reserve for the inhibition of beta-ICa,L than for the activation of IKAdo. Atrial myocytes were pretreated with vehicle (control) or the irreversible A1 adenosine receptor antagonist 8-cyclopentyl-3-[3-[[4-(fluorosulfonyl)benzoyl]oxy]propyl]-1-propylxa nthine (FSCPX) (10 and 50 nM) for 30 min, and after a 60-min washout period, concentration-response curves were determined for the adenosine-induced activation of IKAdo and inhibition of beta-ICa,L. Pretreatment of atrial myocytes with 10 nM FSCPX reduced the maximal activation of IKAdo by 60% (7.9 +/- 0.2 to 3.2 +/- 0.1 pA/pF). In contrast, a higher concentration of FSCPX (50 nM) was required to reduce the maximal inhibition of beta-ICa,L by 39% (95 +/- 4% to 58. 7 +/- 5.6%) and caused a 15-fold increase in the EC50 value of adenosine. Values of the equilibrium dissociation constant (KA) for adenosine to activate IKAdo and inhibit beta-ICa,L, estimated according to the method of Furchgott, were 2.7 and 5.6 microM, respectively. These values were used to determine the relationship between adenosine receptor occupancy and response. Half-maximal and maximal activations of IKAdo required occupancies of 40% and 98% of A1 adenosine receptors, respectively. In contrast, occupancies of only 4% and 70%, respectively, of A1 adenosine receptors were sufficient to cause half-maximal and maximal inhibitions of beta-ICa, L. Consistent with this result, a partial agonist of the A1 adenosine receptor SHA040 inhibited beta-ICa,L by 60 +/- 3.5% but activated IKAdo by only 18.1 +/- 2.5%. The results indicate that the A1 adenosine receptor is coupled more efficiently to an inhibition of beta-ICa,L than to an activation of IKAdo.