Updating the Foodbot Factory serious game with new interactive engaging features and enhanced educational content.

Serious games (i.e., digital games designed for educational purposes) can foster positive learning attitudes and are increasingly used as educational tools. Foodbot Factory is a serious game application (app) that helps children learn about healthy eating based on Canada's Food Guide principles and has demonstrated to increase nutrition knowledge among this group. This paper describes the process followed to expand Foodbot Factory's educational content and integrate immersive technologies and innovative features into the app. The revision process, which was guided by the Obesity-Related Behavioral Intervention Trials model, included the following phases: first, an interdisciplinary team of nutrition scientists, education experts, and computer scientists analyzed data from the original pilot study, recently published literature, and feedback from stakeholders to define areas to improve Foodbot Factory. The five original Foodbot Factory modules were evaluated by the team during weekly meetings, where the educational content, interactive features, and other elements that required updates (e.g., aesthetics and accessibility) were identified. Second, prototypes were created and refined until a final version of Foodbot Factory was approved. Nineteen children tested the updated Foodbot Factory and found it "easy to use" (89%) and "fun" (95%). The new version of Foodbot Factory contains 19 learning objectives, including 13 original and six new objectives. Interactive engagement features in the updated Foodbot Factory included augmented reality incorporated into two learning modules; new mini-games were created, including a memory game; an overhaul of the aesthetics; (e.g., new food images); and accessibility features were included to support users with cognitive and vision disabilities.

Sustained aryl hydrocarbon receptor activity attenuates liver regeneration.

In hepatocyte-derived cell lines, either loss of aryl hydrocarbon receptor (AhR) function or treatment with a persistent AhR agonist such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt G1 phase cell cycle progression. The present study used liver regeneration to explore mechanistically how AhR activity modulates hepatocyte proliferation in vivo. Treatment of mice with 20 mug/kg TCDD 1 day before 70% partial hepatectomy (PH) resulted in a 50 to 75% suppression in liver regeneration. Impaired proliferation was not associated with changes in levels of interleukin-6 or tumor necrosis factor-alpha, which prime quiescent hepatocytes to enter G1 phase. In fact, administration of TCDD 12 h after PH, a period well beyond the priming phase, still induced the G1 arrest. Decreased proliferation in TCDD-treated mice correlated with reduced cyclin-dependent kinase-2 (CDK2) activity, a pivotal regulator of G1/S phase transition. In contrast to observations made in cell culture, suppressed CDK2 activity was not strictly associated with increased binding of the CDK2 inhibitors p21Cip1 or p27Kip1. However, TCDD decreased levels of cyclin E binding to CDK2, despite normal cyclin E expression. The evidence also suggests that TCDD-induced hepatic growth arrest depends upon sustained AhR activity because transient AhR activation in response to endogenous queues failed to suppress the regenerative response. These findings establish a functional role for the AhR in regulating normal cell cycle control during liver regeneration.

Polycystin-2 accelerates Ca2+ release from intracellular stores in Caenorhabditis elegans.

Polycystin-2, a member of the TRP family of calcium channels, is encoded by the human PKD2 gene. Mutations in that gene can lead to swelling of nephrons into the fluid-filled cysts of polycystic kidney disease. In addition to expression in tubular epithelial cells, human polycystin-2 is found in muscle and neuronal cells, but its cell biological function has been unclear. A homologue in Caenorhabditis elegans is necessary for male mating behavior. We compared the behavior, calcium signaling mechanisms, and electrophysiology of wild-type and pkd-2 knockout C. elegans. In addition to characterizing PKD-2-mediated aggregation and mating behaviors, we found that polycystin-2 is an intracellular Ca(2+) release channel that is required for the normal pattern of Ca(2+) responses involving IP(3) and ryanodine receptor-mediated Ca(2+) release from intracellular stores. Activity of polycystin-2 creates brief cytosolic Ca(2+) transients with increased amplitude and decreased duration. Polycystin-2, along with the IP(3) and ryanodine receptors, acts as a major calcium-release channel in the endoplasmic reticulum in cells where rapid calcium signaling is required, and polycystin-2 activity is essential in those excitable cells for rapid responses to stimuli.