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We present a fatal case of pilsicainide poisoning. Quantitative toxicological analysis revealed that the concentrations of pilsicainide in femoral blood and urine samples were 17.5 μg/mL and 136.9 μg/mL, respectively. No morphological changes due to poisoning were observed. Based on the autopsy findings, results of the toxicological examination, and investigation by the authorities, we concluded that the cause of death was due to pilsicainide poisoning.

COA-Cl, a novel adenosine-like nucleic acid analog, has recently been shown to exert neuroprotective effects and to increase dopamine levels both in vivo and in vitro. Therefore, we hypothesized that COA-Cl could protect dopaminergic neurons against toxic insults. Thus, the present study aimed to investigate the protective effects of COA-Cl against hydrogen peroxide (H 2 O 2 )-and 6-hydroxydopamine (6-OHDA)induced toxicity in PC12 cells, and to elucidate the possible mechanisms. PC12 cells were incubated with COA-Cl (100 µM) with or without H 2 O 2 or 6-OHDA (200 µM) for 24 h. Exposure to H 2 O 2 resulted in a decrease in cell viability in a dose-dependent manner. H 2 O 2 enhanced lactate dehydrogenase (LDH) release, reactive oxygen species (ROS) production and caspase-3 activity, and decreased superoxide dismutase (SOD) activity and the Bcl-2/Bax protein ratio. H 2 O 2 also triggered apoptosis as measured by TUNEL analysis. However, treatment with COA-Cl attenuated the decrease in cell viability, SOD activity and the Bcl-2/Bax ratio caused by H 2 O 2 . In addition, COA-Cl attenuated the increase in LDH release, ROS production, caspase-3 activity and apoptosis. 6-OHDA also dose-dependently decreased cell viability and the Bcl-2/Bax ratio, and increased LDH release. However, COA-Cl greatly protected PC12 cells against the toxicity caused by 6-OHDA, as evidenced by an increase in cell viability and the Bcl-2/Bax ratio, and a decrease in LDH release. Our results are the rst to demonstrate that COA-Cl potentially protects PC12 cells against toxicity induced by H 2 O 2 and 6-OHDA, implying that COA-Cl could be a promising neuroprotective agent for the treatment of Parkinson's disease.

A case of fatal poisoning involving multiple psychotropic drugs is presented. Quantitative toxicological analysis showed femoral blood concentrations of pentobarbital, phenobarbital, duloxetine, acetaminophen and tramadol were 10.39, 22.57, 0.22, 0.61 and 0.22 μg/ml, respectively. We concluded that the death was due to the additive effects of two barbiturates. As both pentobarbital and phenobarbital act on gamma-aminobutyric acid (GABA) receptors, central nervous system activity was suppressed, causing respiratory depression. Additive pharmacological effects should be considered in cases of massive ingestion of multiple drugs.