The Promise and Realities of the Use of Cyber Technologies for Promoting Research in Public STEM Museum Experiences

Cyberlab at OSU Final Report.A seven-year effort funded by the United States’ National Science Foundation and the Oregon Sea Grant College Program sought to identify and deploy in a public STEM museum setting a suite of digital tools for collecting and supporting analysis of data on the use of the setting in near real time and as evidence for in situ learning. In addition to full-museum camera coverage and data collection, five exhibit-based research platforms were developed to allow for collection of linked video, audio, and digital input (keystroke, touch screen manipulation) data at particular locations in the museum. A further effort explored the use of social media data mining tools as well as apps for research on how learners create continuity across STEM learning experiences distributed temporally and geographically. Returns on investment for research on informal learning were proven to be high with signifiant gains for researchers working with the museum and for building research partnerships with other museums and informal STEM learning environments (e.g., Maker Faires, public exhibits, tourism in marine environments), but return on investment for museum operations and programmatic advancement were relatively minor. While the project proved that a public museum can successfully employ current video-based, cyber-linked technologies to document and study learning outside of a laboratory setting, it also demonstrated that such activity is most likely beyond the budgetary and information technology capacity of most public institutions. However, the project also piloted and provided proof of concept for smaller, mobile efforts using many of the same technologies and tools in scaled-down but efficient research and evaluation efforts.Keywords: Cyberlearning; Informal Learning Environments; STEM; Video-based Researc

FKS Mutations and Elevated Echinocandin MIC Values among Candida glabrata Isolates from U.S. Population-Based Surveillance ▿

Candida glabrata is the second leading cause of candidemia in the United States. Its high-level resistance to triazole antifungal drugs has led to the increased use of the echinocandin class of antifungal agents for primary therapy of these infections. We monitored C. glabrata bloodstream isolates from a population-based surveillance study for elevated echinocandin MIC values (MICs of ≥0.25 μg/ml). From the 490 C. glabrata isolates that were screened, we identified 16 isolates with an elevated MIC value (2.9% of isolates from Atlanta and 2.0% of isolates from Baltimore) for one or more of the echinocandin drugs caspofungin, anidulafungin, and micafungin. All of the isolates with elevated MIC values had a mutation in the previously identified hot spot 1 of either the glucan synthase FKS1 (n = 2) or FKS2 (n = 14) gene. No mutations were detected in hot spot 2 of either FKS1 or FKS2. The predominant mutation was mutation of FKS2-encoded serine 663 to proline (S663P), found in 10 of the isolates with elevated echinocandin MICs. Two of the mutations, R631G for FKS1 and R665G for FKS2, have not been reported previously for C. glabrata. Multilocus sequence typing indicated that the predominance of the S663P mutation was not due to the clonal spread of a single sequence type. With a rising number of echinocandin therapy failures reported, it is important to continue to monitor rates of elevated echinocandin MIC values and the associated mutations

Declining incidence of candidemia and the shifting epidemiology of Candida resistance in two US metropolitan areas, 2008-2013: results from population-based surveillance.

Recent reports have demonstrated a decline in bacterial bloodstream infections (BSIs) following adherence to central line insertion practices; however, declines have been less evident for BSIs due to Candida species.We conducted active, population-based laboratory surveillance for candidemia in metropolitan Atlanta, GA and Baltimore, MD over a 5-year period. We calculated annual candidemia incidence and antifungal drug resistance rates.We identified 3,848 candidemia cases from 2008-2013. Compared with 2008, candidemia incidence per 100,000 person-years decreased significantly by 2013 in both locations (GA: 14.1 to 9.5, p<0.001; MD: 30.9 to 14.4, p<0.001). A total of 3,255 cases (85%) had a central venous catheter (CVC) in place within 2 days before the BSI culture date. In both locations, the number of CVC-associated cases declined (GA: 473 to 294; MD: 384 to 151). Candida albicans (CA, 36%) and Candida glabrata (CG, 27%) were the most common species recovered. In both locations, the proportion of cases with fluconazole resistance decreased (GA: 8.0% to 7.1%, -10%; MD: 6.6% to 4.9%, -25%), while the proportion of cases with an isolate resistant to an echinocandin increased (GA: 1.2% to 2.9%, +147%; MD: 2.0% to 3.5%, +77%). Most (74%) echinocandin-resistant isolates were CG; 17 (<1%) isolates were resistant to both drug categories (multidrug resistant [MDR], 16/17 were CG). The proportion of CG cases with MDR Candida increased from 1.8% to 2.6%.We observed a significant decline in the incidence of candidemia over a five-year period, and increases in echinocandin-resistant and MDR Candida. Efforts to strengthen infection control practices may be preventing candidemia among high-risk patients. Further surveillance for resistant Candida is warranted

Lysophosphatidic acid stimulates urokinase receptor (uPAR/CD87) in ovarian epithelial cancer cells

Lysophosphatidic acid (LPA) is a bioactive lipid positively linked with ovarian cancer progression. The multi-functional urokinase receptor (uPAR), a cell-surface glycoprotein, binds and facilitates activation of uPA and laterally regulates integrin and tyrosine kinase receptor activities in promotion of cell migration and invasion. We hypothesized that LPA stimulates uPAR expression and activity in ovarian epithelial cancer cells. Materials and Methods: Ovarian epithelial cancer cell lines OVCA 429 and OVCA 433 were stimulated with LPA and examined for uPAR mRNA expression and protein localization. uPA binding to OVCA plasma membranes was measured through enzymatic analysis of affinity-isolated cell-surface proteins. Results: LPA drove cell-surface uPAR aggregation and mRNA expression concomitant with increased cell-surface binding of uPA. Both control and LPA-stimulated uPAR expression and uPA cell-surface association involved phosphatidylinositol 3-kinase, but not p38 or p42 mitogen-activated protein kinase, signaling. Conclusion: These data provide mechanistic insight into ovarian epithelial cancer cell progression by demonstrating that LPA drives uPAR expression and uPA binding

Annual candidemia incidence rates per 100,000 person-years, by year and age-group in the Metropolitan Atlanta area.

<p>Annual candidemia incidence rates per 100,000 person-years, by year and age-group in the Metropolitan Atlanta area.</p

Annual candidemia incidence rates per 100,000 person-years, by year and location, 2008–2013.

<p>Annual candidemia incidence rates per 100,000 person-years, by year and location, 2008–2013.</p