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Educational program development in the format of continuing education or certificate is needed to improve pharmacists' education, confidence and training needs in PGx.

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Several studies mentioned the association of oxidative stress and neuroinflammation with Parkinson's disease (PD). In the MPTP‐injured PC12 cells, a rat model of PD, MPTP induces cell death through complex I inhibition in the mitochondria, increases the production of nitric oxide (NO) and pro‐inflammatory mediators such as IL‐1beta and TNF‐alpha. This study, investigated the mechanisms underlying the neuroprotective effect of two anti‐inflammatory drugs, Fisetin and Ibuprofen in MPTP‐induced PC12. Cell viability was measured by MTT assay, IL‐1beta levels were quantified by ELISA, TNF‐alpha expression was assessed by western blot, and NO levels were also evaluated. PC12 cells were pretreated with varying doses of fisetin, ibuprofen, or both drugs in combination for 2 hours, prior to MPTP treatment. Pretreatment with fisetin produced a dose‐dependent increase in cell viability, and a dose‐dependent decrease in the expression of TNF‐alpha. Ibuprofen at 2 μg/ml also decreased TNF‐alpha expression in MPTP treated PC12 cells. The combination of both drugs showed a synergistic effect in the inhibition of TNF‐alpha expression. Fisetin also suppressed the production of NO and IL‐1beta in a dose‐dependent manner, and that both drugs combined showed a synergistic effect in suppressing the NO and IL‐1beta production. The present study indicates that fisetin and ibuprofen may provide a promising approach for the treatment of neuroinflammation associated with PD.

Isolated rat hepatocyte couplets were used to study the direct effect of insulin on intracellular Ca2+ homeostasis. Insulin induced a dose-dependent increase in hepatocellular Ca2+ that was gradual, generally monophasic, and reversible. Chelation of extracellular Ca2+ abolished the insulin-induced Ca2+ response, and this suppression was not related to an effect on insulin binding, as indicated by displacement studies. We thus tested the effect of several Ca2+ channel inhibitors on insulin-induced Ca2+ influx. Verapamil at 20 or 200 microM was without effect, whereas 500 microM nickel and 50 microM gadolinium strongly inhibited insulin-induced Ca2+ entry. Finally, we tested whether insulin-induced Ca2+ movements were implicated in the stimulation of mitogen-activated protein kinase (MAPK) activity, which we measured with the use of an immune-complex assay. Verapamil was without effect on the insulin-dependent stimulation of p44mapk activity, whereas addition of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, nickel, or gadolinium strongly inhibited the effect of the peptide hormone. Our results indicate that insulin triggers Ca2+ influx into hepatocytes, possibly through the opening of channels on the plasma membrane, and that this effect is important for insulin activation of MAPK.