Sonolytic and silent polymerization of methacrlyic acid butyl ester catalyzed by a new onium salt with bis-active sites in a biphasic system--a comparative investigation.

Currently, ingenious new analytical and process experimental techniques which are environmentally benign techniques, viz., ultrasound irradiation, have become immensely popular in promoting various reactions. In this work, a novel soluble multi-site phase transfer catalyst (PTC) viz., 1,4-bis-(propylmethyleneammounium chloride)benzene (BPMACB) was synthesized and its catalytic efficiency was assessed by observing the kinetics of sonolytic polymerization of methacrylic acid butyl ester (MABE) using potassium persulphate (PPS) as an initiator. The ultrasound-multi-site phase transfer catalysis (US-MPTC)-assisted polymerization reaction was compared with the silent (non-ultrasonic) polymerization reaction. The effects of the catalyst and various reaction parameters on the catalytic performance were in detail investigated by following the kinetics of polymerization of MABE in an ethyl acetate-water biphasic system. From the detailed kinetic investigation we propose a plausible mechanism. Further the kinetic results demonstrate clearly that ultrasound-assisted phase-transfer catalysis significantly increased the reaction rate when compared to silent reactions. Notably, this environmentally benign and cost-effective process has great potential to be applied in various polymer industries.

Functional identification of an outwardly rectifying pH- and anesthetic-sensitive leak K(+) conductance in hippocampal astrocytes.

Astrocytes function as spatial K(+) buffers by expressing a rich repertoire of K(+) channels. Earlier studies suggest that acid-sensitive tandem-pore K(+) channels, mainly TWIK-related acid-sensitive K(+) (TASK) channels, mediate part of the passive astroglial membrane conductance. Here, using a combination of electrophysiology and pharmacology, we investigated the presence of TASK-like conductance in hippocampal astrocytes of rat brain slices. Extracellular pH shifts to below 7.4 (or above 7.4) induced a prominent inward (or outward) current in astrocytes in the presence of tetrodotoxin, a Na(+) channel blocker, and 4,4'-diisothiocyanatostilbene-2,2'-disulfonate, a co-transporter blocker. The pH-sensitive current was insensitive to quinine, a potent blocker of tandem-pore K(+) channels including TWIK-1 and TREK-1 channels. Voltage-clamp analysis revealed that the pH-sensitive current exhibited weak outward rectification with a reversal potential of -112 mV, close to the Nernst equilibrium potential for K(+) . Furthermore, the current-voltage relationship was well fitted with the Goldman-Hodgkin-Katz current equation for the classical open-rectifier 'leak' K(+) channel. The pH-sensitive K(+) current was potentiated by TASK channel modulators such as the volatile anesthetic isoflurane but depressed by the local anesthetic bupivacaine. However, unlike TASK channels, the pH-sensitive current was insensitive to Ba(2+) and quinine. Thus, the molecular identity of the pH-sensitive leak K(+) channel is unlikely to be attributable to TASK channels. Taken together, our results suggest a novel yet unknown leak K(+) channel underlying the pH- and anesthetic-sensitive background conductance in hippocampal astrocytes.