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Competition is a key element in many educational games and is often adopted by educators in an effort to motivate and excite their students. Yet, the use of academic competition in educational institutions remains the subject of much debate. Opponents argue that academic competition causes an increase in student anxiety and divides their attention. However, if the contexts of academic competition are defined, could the inclusion of a game-like competition in a university course be a viable and beneficial method of engaging students? Students (n?=?67) were recruited from an undergraduate human anatomy course at Western University. Using a crossover design, students were exposed to a competitive tournament either at the time of their first term test or second term test. The anatomical knowledge of participating students was assessed prior to the start of the study using a baseline anatomy test. Following treatment with an online competitive anatomy tournament, student's term test grades and final course grades were analyzed. Both the second term test scores (F(2,64)?=?3.743, P?=?0.029) and overall course grades (F(2,64)?=?3.356, P?=?0.041) were found to be significantly different (P?

Neoplastic transformation is frequently associated with a loss of gap junctional intercellular communication and reduced expression of connexins. The introduction of connexin genes into tumor cells reverses the proliferative characteristics of such cells. However, there is very little comparative information on the effects of different connexins on cancer cell growth. We hypothesized that Cx26, Cx32, or Cx43 would display differential growth suppression of C6 glioma cells and uniquely modulate the bystander effect following transduction of C6 cells with HSVtk followed by suicide gene therapy. The bystander phenomenon is the death of a greater number of tumor cells than are expressing the HSVtk gene, presumably due to the passage of toxic molecules through gap junction channels. To test this hypothesis, we used retroviral vectors to infect C6 glioma cells producing connexin-expressing and HSVtk-expressing cell lines. All three connexin-expressing cell lines grew significantly slower than GFP-infected or native C6 cells. Cx32 and Cx26 were significantly more effective at mediating the bystander effect in cocultures of C6-connexin cells with C6-HSVtk cells. These studies indicate that connexins have unique properties that contribute to their tumor suppressive function. [ABSTRACT FROM AUTHOR]

Competing Interests: None declared.

The function of gap junctions is regulated by the phosphorylation state of their connexin subunits. Numerous growth factors are known to regulate connexin phosphorylation; however, the effect of nerve growth factor on gap junction function is not understood. The phosphorylation of connexin subunits is a key event during many aspects of the lifecycle of a connexin, including open/close states, assembly/trafficking, and degradation, and thus affects the functionality of the channel. PC12 cells infected with connexin43 (Cx43) retrovirus were used as a neuronal model to characterize the signal transduction pathways activated by nerve growth factor (NGF) that potentially affect the functional state of Cx43. Immunoblot analysis demonstrated that Cx43 and the mitogen-activated protein kinase (MAPK), ERK-1/2, were phosphorylated in response to TrkA activation via NGF and that phosphorylation could be prevented by treatment with the MEK-1/2 inhibitor U0126. The effects of NGF on gap junction intercellular communication were examined by monitoring fluorescence recovery after photobleaching PC12-Cx43 cells preloaded with calcein. Fluorescence recovery in the photobleached area increased after NGF treatment and decreased when pretreated with the MEK-1/2 inhibitor U0126. These data are the first to show a direct signaling link between neurotrophins and the phosphorylation of connexin proteins through the MAPK pathway resulting in increased gap junctional intercellular communication. Neurotrophic regulation of connexin activity provides a novel mechanism of regulating intercellular communication between neurons during nervous system development and repair.