In Search of Quality: Using Quality Matters to Analyze the Quality of Massive, Open, Online Courses (MOOCs)

The concept of the massive, open, online course (MOOC) is not new, but high-profile initiatives have moved MOOCs into the forefront of higher education news over the past few years. Members of institutions of higher education have mixed feelings about MOOCs, ranging from those who want to offer college credit for the successful completion of MOOCs to those who fear MOOCs are the end of the university as we know it. We set forth to investigate the quality of MOOCs by using the Quality Matters quality control framework. In this article, we present the results of our inquiry, with a specific focus on the implications the results have on day-to-day practice of designing online courses

Investigating Peer Review as an Intentional Learning Strategy to Foster Collaborative Knowledge-Building in Students of Instructional Design

Peer review has been advocated for as an intentional strategy to support the knowledge and skill attainment of adult learners preparing for professional practice, including those students preparing for instructional design and technology practice. The purposes of this article are to discuss the practical application of peer review as an instructional strategy by articulating its use in both face-to-face and online Instructional Design courses and to formulate directions for future research on the use of peer review in instructional practice. Findings from a literature review of student-to-student peer review and the authors\u27 experiences with the use of peer review in Instructional Design courses are used to foster a discussion that interweaves both important scholarly and practical elements

STEM Education in Rural Schools: Implications of Untapped Potential

A large number of students in American public schools attend rural schools. In this paper, the authors explore rural science, technology, engineering, and math (STEM) education and the issues associated with STEM education for students, teachers, and parents in rural communities. Characteristics of rural STEM education are examined to highlight unique considerations for this context. The authors conclude with the recommendation that more research is needed that specifically addresses rural STEM education

Resolvin D1 and Aspirin-Triggered Resolvin D1 Regulate Histamine-stimulated Conjunctival Goblet Cell Secretion

Resolution of inflammation is an active process mediated by pro-resolution lipid mediators. Since resolvin (Rv) D1 is produced in the cornea, pro-resolution mediators could be effective in regulating inflammatory responses to histamine in allergic conjunctivitis. Two key mediators of resolution are the D-series resolvins RvD1 or aspirin-triggered RvD1 (AT-RvD1). We used cultured conjunctival goblet cells to determine whether histamine actions can be terminated during allergic responses. We found cross-talk between two types of G protein-coupled receptors, as RvD1 interacts with its receptor GPR32 to block histamine-stimulated H1 receptor increases in intracellular [Ca2+] ([Ca2+]i) preventing H1 receptor-mediated responses. In human and rat conjunctival goblet cells RvD1 and AT-RvD1 each block histamine-stimulated secretion by preventing its increase in [Ca2+]i and activation of extracellular regulated protein kinase (ERK)1/2. We suggest that D-series resolvins regulate histamine responses in the eye and offer new treatment approaches for allergic conjunctivitis or other histamine-dependent pathologies

Salinity and temperature balances at the SPURS central mooring during fall and winter

Author Posting. © The Oceanography Society, 2015. This article is posted here by permission of The Oceanography Society for personal use, not for redistribution. The definitive version was published in Oceanography 28, no. 1 (2015): 56-65, doi:10.5670/oceanog.2015.06.One part of the Salinity Processes in the Upper-ocean Regional Study (SPURS) field campaign focused on understanding the physical processes affecting the evolution of upper-ocean salinity in the region of climatological maximum sea surface salinity in the subtropical North Atlantic (SPURS-1). An upper-ocean salinity budget provides a useful framework for increasing this understanding. The SPURS-1 program included a central heavily instrumented mooring for making accurate measurements of air-sea surface fluxes, as well as other moorings, Argo floats, and gliders that together formed a dense observational array. Data from this array are used to estimate terms in the upper-ocean salinity and heat budgets during the SPURS-1 campaign, with a focus on the first several months (October 2012 to February 2013) when the surface mixed layer was becoming deeper, fresher, and cooler. Specifically, we examine the salinity and temperature balances for an upper-ocean mixed layer, defined as the layer where the density is within 0.4 kg m–3 of its surface value. The gross features of the evolution of upper-ocean salinity and temperature during this fall/winter season are explained by a combination of evaporation and precipitation at the sea surface, horizontal transport of heat and salt by mixed-layer currents, and vertical entrainment of fresher, cooler fluid into the layer as it deepened. While all of these processes were important in the observed seasonal (fall) freshening at this location in the salinity-maximum region, the variability of salinity on monthly-to-intraseasonal time scales resulted primarily from horizontal advection.J.T. Farrar, A.J. Plueddemann, J.B. Edson, and the deployment of the central mooring were supported by NASA grant NNX11AE84G. L. Rainville, C. Lee, C. Eriksen, and the Seaglider program were supported by NASA grant NNX11AE78G. R. Schmitt was supported by NSF grant OCE-1129646. B. Hodges and D. Fratantoni were supported by NASA grant NNX11AE82G. The Prawler moorings were funded by PMEL. The data analysis was also supported by NASA grant NNX14AH38G

Regional and cellular gene expression changes in human Huntington's disease brain

Huntington's disease (HD) pathology is well understood at a histological level but a comprehensive molecular analysis of the effect of the disease in the human brain has not previously been available. To elucidate the molecular phenotype of HD on a genome-wide scale, we compared mRNA profiles from 44 human HD brains with those from 36 unaffected controls using microarray analysis. Four brain regions were analyzed: caudate nucleus, cerebellum, prefrontal association cortex [Brodmann's area 9 (BA9)] and motor cortex [Brodmann's area 4 (BA4)]. The greatest number and magnitude of differentially expressed mRNAs were detected in the caudate nucleus, followed by motor cortex, then cerebellum. Thus, the molecular phenotype of HD generally parallels established neuropathology. Surprisingly, no mRNA changes were detected in prefrontal association cortex, thereby revealing subtleties of pathology not previously disclosed by histological methods. To establish that the observed changes were not simply the result of cell loss, we examined mRNA levels in laser-capture microdissected neurons from Grade 1 HD caudate compared to control. These analyses confirmed changes in expression seen in tissue homogenates; we thus conclude that mRNA changes are not attributable to cell loss alone. These data from bona fide HD brains comprise an important reference for hypotheses related to HD and other neurodegenerative disease

Mutant huntingtin's effects on striatal gene expression in mice recapitulate changes observed in human Huntington's disease brain and do not differ with mutant huntingtin length or wild-type huntingtin dosage

To test the hypotheses that mutant huntingtin protein length and wild-type huntingtin dosage have important effects on disease-related transcriptional dysfunction, we compared the changes in mRNA in seven genetic mouse models of Huntington's disease (HD) and postmortem human HD caudate. Transgenic models expressing short N-terminal fragments of mutant huntingtin (R6/1 and R6/2 mice) exhibited the most rapid effects on gene expression, consistent with previous studies. Although changes in the brains of knock-in and full-length transgenic models of HD took longer to appear, 15- and 22-month CHL2Q150/Q150, 18-month HdhQ92/Q92 and 2-year-old YAC128 animals also exhibited significant HD-like mRNA signatures. Whereas it was expected that the expression of full-length huntingtin transprotein might result in unique gene expression changes compared with those caused by the expression of an N-terminal huntingtin fragment, no discernable differences between full-length and fragment models were detected. In addition, very high correlations between the signatures of mice expressing normal levels of wild-type huntingtin and mice in which the wild-type protein is absent suggest a limited effect of the wild-type protein to change basal gene expression or to influence the qualitative disease-related effect of mutant huntingtin. The combined analysis of mouse and human HD transcriptomes provides important temporal and mechanistic insights into the process by which mutant huntingtin kills striatal neurons. In addition, the discovery that several available lines of HD mice faithfully recapitulate the gene expression signature of the human disorder provides a novel aspect of validation with respect to their use in preclinical therapeutic trial