Through different learning portals, computer-assisted assessment (CAA) tools have improved considerably over the past few decades. In a CAA community, these tools are categorised into types of questions, types of testing, and types of assessment. Most of these provide the assessment of multiple-choice questions, true and false questions, or matching questions. Other CAA tools evaluate short and long essay questions, each of which different grading methods and techniques in terms of style and content have. However, due to the complexity involved in analysing free text writing, the development and evaluation of accurate, easy to use, and effective tools is questionable. This research proposes a new contextual framework as a novel approach to the investigation of a new CAA tool which auto-generates feedback on project proposals. This research follows a Design Science Research paradigm to achieve and evaluate the accuracy, ease of use, and effectiveness of the new tool in the computer science domain in higher education institutes. This is achieved in three interrelated cycles:(1) based on the existent literature on this topic and an exploratory study on the currently available approaches to the provision of feedback on final year project proposals, a proposed framework to auto-generate feedback on any electronically submitted coursework is constructed in order to gain a clear understanding on how such a CAA tool might work; (2) a contextual framework based on the proposed framework for final year project proposals is constructed by considering both the style and content of the free text and using different text mining techniques; and (3) the accuracy, easy to use, and effectiveness of the implemented web-based CAA application named Feedback Automated Tool (FEAT)is evaluated based on the contextual framework. This research applies CAA and text mining techniques to identify and model the key elements of the framework and its components in order to enable the development and evaluation of a novel CAA contextual framework which can be utilised for auto-generating accurate, easy to use, and effective feedback on final year project proposals.

Inflammation or nerve injury sensitizes several populations of nociceptive neurons in the dorsal horn of the spinal cord, including those that express the neuropeptide Y (NPY) Y1 receptor (Y1R). Our overall hypothesis is that after tissue or nerve injury, these Y1R-expressing neurons enter a state of latent sensitization (LS) that contributes to vulnerability to the development of chronic pain; furthermore, LS is under the tonic inhibitory control of endogenous Y1R signaling. First, we evaluated the intracellular signaling pathways that become activated in Y1R-expressing neurons and participate in LS. To do this, we established behavioral models of inflammatory or neuropathic pain, allowed pain hypersensitivity to resolve, and then during this period of pain remission we administered the Y1R receptor antagonist, BIBO3304, by intrathecal injection. As observed previously with mu-opioid receptor antagonists/inverse agonists, we found that BIBO3304 reinstated pain hypersensitivity via an N-methyl-D-aspartate receptor (NMDAR)- and adenylyl cyclase type 1 (AC1)-dependent mechanism. Our subsequent behavioral pharmacological experiments then established two signaling pathways downstream of AC1 that maintain LS. The first pathway involves protein kinase A (PKA) and transient receptor potential cation channel A1 (TRPA1) and channel V1 (TRPV1). The second pathway involves exchange proteins activated by cAMP (Epac 1 and Epac 2). We next found that nerve injury decreases the co-expression of Y1R with markers of excitatory interneurons, suggesting that Y1R-expressing neurons acquire a pain-enhancing phenotype after peripheral nerve injury. In a separate set of experiments that utilized Y1R-receptor internalization as an index of NPY release, we found that nerve injury increased stimulus-evoked NPY release. We conclude that injury induces pain-facilitatory mechanisms of LS in the dorsal horn involving PKA→TRPA1 and PKA→TRPV1 at the central terminals of primary afferent neurons. Whether Epac mechanisms are located on these same presynaptic terminals and/or at Y1R-expressing excitatory interneurons remain to be determined. We also conclude that injury-induced LS is masked by a compensatory up-regulation of spinal NPY release that tonically inhibits pain. These results present a novel mechanism of injury-induced LS and endogenous control of the transition from acute to chronic pain by the NPY-Y1R system. Our work sheds light on novel targets for the treatment of chronic pain.