Examination of 125 insulin pens used in hospitals revealed hemoglobin in 1 pen and at least one cell in another 6 pens. The nine detected cells consisted of four squamous epithelial cells, four macrophages, and one RBC.

Objective. To examine whether playing a board game can assist PharmD students in learning autonomic nervous system (ANS) pharmacology. Design. Of 72 students enrolled in a required second-year pharmacology course, 22 students volunteered to play the board game, which was followed by an in-class examination consisting of 42 ANS questions (ANSQs) and 8 control questions (CTLQs). Participants were given a pretest and a posttest to assess immediate educational improvement. Participants' scores for pretest, posttest, in-class examination, and ANSQs were compared. Also, scores for examination, ANSQs, and CTLQs were compared between board game participants (PART) and nonparticipating classmates (NPART). Assessment. Board game participants scored progressively higher between the pretest, posttest, examination, and ANSQs. Additionally, PART scores were higher than NPART scores for examination and ANSQs. Difference between PART and NPART CTLQ scores was not significant. Conclusion. A board game can assist PharmD students in learning ANS pharmacology.

The cJun N-terminal kinase (JNK)-signaling pathway is activated in response to a variety of stimuli, including environmental insults, and has been implicated in neuronal apoptosis. In this study, we investigated the role that the JNK pathway plays in neurotoxicity caused by thimerosal, an ethylmercury-containing preservative. SK-N-SH cells treated with thimerosal (0-10 microM) showed an increase in the phosphorylated (active) form of JNK and cJun with 5 and 10 microM thimerosal treatment at 2 and 4 h. To examine activator protein-1 (AP-1) transcription, cells were transfected with a pGL2 vector containing four AP-1 consensus sequences and then treated with thimerosal (0-2.5 microM) for 24 h. Luciferase studies showed an increase in AP-1 transcriptional activity upon thimerosal administration. To determine the components of the AP-1 complex, cells were transfected with a dominant negative to either cFos (A-Fos) or cJun (TAM67). Reporter analysis showed that TAM67, but not A-Fos, decreased AP-1 transcriptional activity, indicating a role for cJun in this pathway. To assess which components are essential to apoptosis, cells were treated with a cell-permeable JNK inhibitor II (SP600125) or transfected with TAM67, and the downstream effectors of apoptosis were analyzed. Cells pretreated with SP600125 showed decreases in activation of caspases 9 and 3, decreases in degradation of poly(ADP-ribose) polymerase (PARP), and decreased levels of proapoptotic Bim, in comparison to cells treated with thimerosal alone. However, cells transfected with TAM67 showed no changes in those same components. Taken together, these results indicate that thimerosal-induced neurotoxicity occurs through the JNK-signaling pathway, independent of cJun activation, leading ultimately to apoptotic cell death.

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