An Educational Setting to improve Students’ Understanding of Fundamental Computer Architecture Concepts

This paper presents an educational setting that attempts to enhance students’ understanding and facilitate students’ linking-inferencing skills. The proposed setting is structured in three stages. The first stage intends to explore students’ prior knowledge. The second stage aims to help students tackle their difficulties and misconceptions and deepen their understanding of the topics under study. This is attempted through individual student engagement in suitably-designed activities and relative feedback. As recorded in previous research, students’ difficulties feedback on the material development. The third stage of the educational setting exploits social interaction to help students reorganize their knowledge of the concepts under study. The web-based application of the proposed educational setting indicated improvement in first-year Computer Science (CS) students’ understanding of fundamental Computer Architecture concepts and progress in students’ linking-inference skills. These results encourage integration in the instructional process of interventions designed according to the proposed setting in order to support and enhance students’ understanding of troublesome concepts and their interrelations

PERK promotes cancer cell proliferation and tumor growth by limiting oxidative DNA damage

In order to proliferate and expand in an environment with limited nutrients, cancer cells co-opt cellular regulatory pathways that facilitate adaptation and thereby maintain tumor growth and survival potential. The endoplasmic reticulum (ER) is uniquely positioned to sense nutrient deprivation stress and subsequently engage signaling pathways that promote adaptive strategies. As such, components of the ER stress-signaling pathway represent potential anti-neoplastic targets. However, recent investigations into the role of the ER resident protein kinase PERK have paradoxically suggested both pro- and anti-tumorigenic properties. We have utilized animal models of mammary carcinoma to interrogate PERK contribution in the neoplastic process. The ablation of PERK in tumor cells resulted in impaired regeneration of intracellular antioxidants and accumulation of reactive oxygen species triggering oxidative DNA damage. Ultimately, PERK deficiency impeded progression through the cell cycle due to the activation of the DNA damage checkpoint. Our data reveal that PERK-dependent signaling is utilized during both tumor initiation and expansion to maintain redox homeostasis and thereby facilitates tumor growth