Ultrasound-assisted leaching of spent lithium ion batteries by natural organic acids and H2O2.

Ultrasound-assisted bioacid leaching was examined for the extraction of valuable metals from spent lithium ion batteries (LIBs). In this work, organic acids in lemon juice were used as the leaching agent together with H2O2. Three effective factors, namely solid/liquid (S/L) ratio, lemon juice percentage, and H2O2 volume percentage, were optimized using Response Surface Methodology (RSM). The optimal conditions were found to be 0.98% (w/v) S/L ratio, 57.8% (v/v) lemon juice and 8.07% (v/v) H2O2 in the leaching liquor, achieving recovery of 100% Li, 96% Co and 96% Ni. Furthermore, the individual effects of ultrasound, H2O2 and lemon juice on metal recovery were studied and the results showed that without H2O2 or lemon juice, the metal recovery rates decreased greatly while the absence of ultrasound reduced recovery rates to a much smaller extent, indicating that both H2O2 and lemon juice were essential in the leaching process. The effect of time on the metals recoveries was examined and results showed that Li and Co recovery reached 100% with the leaching time of 35 min. The modified shrinking core modeling results suggested that chemical reaction was the rate controlling step.

Nicotinic acetylcholine receptors of the dorsal hippocampus and the basolateral amygdala are involved in ethanol-induced conditioned place preference.

The purpose of this study was to evaluate whether nicotinic acetylcholine receptors of the dorsal hippocampus and the basolateral amygdala (BLA) can potentiate ethanol response in the conditioned place preference (CPP) paradigm. I.p. administration of different doses of ethanol (0.25-1 g/kg) did not induce CPP. However, the higher dose of the drug (1.5 g/kg i.p.) induced place aversion. Furthermore, microinjection of nicotine (0.5-1 microg/rat) into both CA1 regions (intra-CA1) and the BLA (intra-BLA) did not produce a significant CPP. Interestingly, intra-CA1 or -BLA administration of nicotine plus ethanol (0.5 g/kg) during conditioning phase significantly induced a strong CPP. Microinjection of mecamylamine, the nicotinic acetylcholine receptor antagonist, into the CA1 regions or into the BLA did not alter CPP. However, intra-CA1 or -BLA microinjection of mecamylamine (1-4 microg/rat) reversed the response induced by the microinjection of nicotine (1 microg/rat, intra-CA1 or -BLA) plus ethanol (0.5 g/kg i.p.) in the CPP paradigm. On the other hand, the microinjection of nicotine (0.5-1.5 microg/rat) into the BLA, but not into the CA1 regions before the testing phase potentiated the response of ethanol on the expression of conditioned place preference. Moreover, intra-CA1 administration of nicotine plus ethanol increased the locomotor activity on the test day which was reversed by pretreatment with mecamylamine, while other treatments had no effect on locomotor activity. It can be concluded that the activation of nicotinic acetylcholine receptors of the dorsal hippocampus and the basolateral amygdala can potentiate the ethanol response in the CPP paradigm.