Kimberly E. Arnold

Building institutional capacities and competencies for systemic learning analytics initiatives

The last five years have brought an explosion of research in the learning analytics field. However, much of what has emerged has been small scale or tool-centric. While these efforts are vitally important to the development of the field, in order to truly transform education, learning analytics must scale and become institutionalized at multiple levels throughout an educational system. Many institutions are currently undertaking this grand challenge and this panel will highlight cases from: the University of Wisconsin System, the Society for Learning Analytics Research, the University of New England, and Rio Salado College.

Measuring student success using predictive engine

A basic challenge in delivering global education is improving student success. Institutions of education are increasingly focused on improving graduation and retention rates of their students. In this poster, we describe Student Success System (S3) that can measure student performance starting from the first weeks of the semester and the adoption process for S3 by University of Wisconsin System (UWS).

Student empowerment, awareness, and self-regulation through a quantified-self student tool

The purpose of this paper is to examine the cross institutional use of a quantified-self application called Pattern, which is designed to promote self-regulation and reflective learning in learners. This paper provides a brief look into how learners report spending their time and react to in-app recommendations. Initial data is encouraging; however, there are limitations of Pattern, and additional research and development must be undertaken.

Student perceptions of their privacy in leaning analytics applications

Over the past five years, ethics and privacy around student data have become major topics of conversation in the learning analytics field. However, the majority of these have been theoretical in nature. The authors of this paper posit that more direct student engagement needs to be undertaken, and initial data from institutions beginning this process is shared. We find that, while the majority of respondents are accepting of the use of their data by their institutions, approval varies depending on the proposed purpose of the analytics. There also appear to be notable variations between students enrolled at United Kingdom and American institutions.

P2-377: CSF biomarkers correlate with regional brain volume and fMRI activation patterns in middle-aged adults at risk for Alzheimer’s disease

hippocampal volume were determined by lobar volume alone. In AD, temporal and occipital GM were determined by lobar volume (p 0.05) but not frontal, parietal and hippocampal GM. Conclusion: The finding that lobar WML determined frontal and occipital GM and hippocampal volume in controls suggests that WML can be associated with localized GM atrophy. In CVD, frontal WML determined frontal GM but not GM in other lobes. This suggests that similar to AD, GM atrophy in CVD is determined by cortical pathology, e.g. microinfarcts, rather than remote effects of WML.

The effects of gender on the relationship between body mass index and CSF AB42 and tau levels

the M-CSF receptor (M-CSFR). We previously showed that increasing expression of the M-CSFR on cultured microglia dramatically upregulates microglia M-CSF and IL-1 expression. Objectives: To determine if knockdown of microglial interleukin-1 and M-CSF expression affects NMDA-induced neurotoxicity in a co-culture system. Methods: We used a co-culture model consisting of microglia overexpressing the M-CSFR and hippocampal organotypic cultures treated with the neurotoxin NMDA. To test the importance of microglial IL-1 and M-CSF on neuronal survival, we used an shRNA gene-targeted approach in which we selectively and without toxicity deleted microglial IL-1 or M-CSF expression prior to co-culture assembly. Transfections were performed with the hairpin RNA expression plasmid pGSU6-GFP-shRNA. To quantify neuronal injury, we used propidium iodide as well as FluoroJade staining. Results: We found that when microglia overexpressing the M-CSFR were cocultured with organotypic slices, there was complete protection of neurons from NMDA-induced injury. However, after knockdown of either microglial IL-1 or M-CSF, neuroprotection was abolished. Using TaqMan real-time RT-PCR, we confirmed that the shRNA constructs resulted in a 75% knockdown of cytokine expression. Both M-CSF and IL-1 were necessary for microglial proliferation, but only IL-1 removal also suppressed chemotactic migration of microglia toward the NMDA-injured organotypic culture. Conclusions: These results demonstrate that IL-1 and M-CSF are essential for M-CSFR-induced microglial neuroprotection in a microglial-organotypic hippocampal co-culture system. In AD, increased IL-1 and M-CSF expression by M-CSFR-activated microglia could actually serve to protect, rather than harm neurons. It may be that some inflammatory factors expressed early in AD could be beneficial, so that suppressing inflammation might accelerate rather than prevent disease progression. (Supported by an Alzheimer’s Association New Investigator Award to O.M. and NIH award MH57833).