-Acetaminophen (Paracetamol, APAP) has been widely used for many decades as an analgesic and antipyretic agent but APAP overdose often causes acute adverse reactions, particularly liver damage. The metabolically oxidized form of APAP, N-acetyl-p-benzoquinone imine (NAPQI), is chemically reactive and binds covalently to proteins. Therefore, NAPQI is believed to be the key metabolite that causes hepatotoxicity, especially under conditions of glutathione depletion. Other APAP-induced adverse reactions, such as skin damage, are rare and remain poorly studied. Here, we report a case study of a male patient who presented with an acute swelling skin rash (without hepatotoxicity) caused by therapeutic doses of APAP. Plasma samples were collected at 17 hr after dosing (during the manifestation of symptoms) and at one month (after recovery) and were subjected to LC-MS analysis of NAPQI-adducts. A significant concentration of NAPQI-cysteine adduct (33 pmol/mL) was found together with low concentrations of NAPQI-N-acetylcysteine adduct (2.0 pmol/mL) and NAPQI-glutathione adduct (0.13 pmol/mL). However, the NAPQI-albumin adduct was below the detection limit (below 0.001% modification on albumin) despite a previous report of high concentrations of NAPQI-albumin adduct following acute liver injury. Therefore, the observed APAP-induced skin damage may have had a different cause from APAPinduced liver injury.

The mechanical strain of the neural tissue induced by the implant of neuronal electrode is one of the important factors responsible for the quality and performance of extracellular recording of neuronal activities in the brain because the mechanical strain could kill or inactivate the neurons. In order to evaluate the effect of the implant of neural electrode, we propose a method to estimate the three-dimensional distribution of electrophysiologically active neurons near the electrode based on the multi-site multi-unit recording data. The spatial distribution of the active neurons emerges the region in the neural tissue that could be killed or inactivated by the implant of the electrode. The proposed method will be useful for the in situ assessment of the neural electrode implanted in the brain.

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