Libraries and Museums: Fostering GLAM Collaboration at the University of Iowa

This report outlines the findings of the University of Iowa (UI) Executive Leadership Academy – Higher Education (ELA) project team GLAM1 during the 2017-18 academic year. Team GLAM was charged by the UI Stanley Museum of Art Interim Chair James Leach and UI Librarian John Culshaw with investigating the present state and potential of new collaboration between the Stanley Museum and those UI Libraries with the greatest focus on the visual arts. This report provides the team’s findings, as well as its recommendations for forging new relationships and leveraging the strengths of both types of institution to transform them into places where bold experiments will generate new ideas for research, teaching, and service. Based on our discussions, research, site visits, interviews, and ideation sessions held between October 2017 and April 2018, team GLAM recommends implementation of the following five broad collaborative practices. Full details around these recommendations can be found on pps. 18-20 in the final report: Establish a formal GLAM committee that is empowered to shape an environment on campus where GLAM can flourish and be sustained. Increase opportunities for collaborations across staff positions. Reward and recognize staff and faculty who actively and productively collaborate in GLAM research, teaching, and service activities. Identify and proactively pursue grants and other funding opportunities that support collaborative activities across GLAM. Invest in digitization and joint technologies related to accessibility and discovery. GLAM on the UI campus faces enormous budgetary, technology, and other environmental challenges that are most effectively addressed by broader collaboration across campus, beyond traditional organizational structures and disciplines. By strengthening current collaborations while seeking new ones across campus, the Stanley Museum of Art and the UI Libraries can leverage the strengths of both entities and advance their missions in service of UI’s broader strategic goals

ER Stress Inhibits Liver Fatty Acid Oxidation while Unmitigated Stress Leads to Anorexia-Induced Lipolysis and Both Liver and Kidney Steatosis

The unfolded protein response (UPR), induced by endoplasmic reticulum (ER) stress, regulates the expression of factors that restore protein folding homeostasis. However, in the liver and kidney, ER stress also leads to lipid accumulation, accompanied at least in the liver by transcriptional suppression of metabolic genes. The mechanisms of this accumulation, including which pathways contribute to the phenotype in each organ, are unclear. We combined gene expression profiling, biochemical assays, and untargeted lipidomics to understand the basis of stress-dependent lipid accumulation, taking advantage of enhanced hepatic and renal steatosis in mice lacking the ER stress sensor ATF6α. We found that impaired fatty acid oxidation contributed to the early development of steatosis in the liver but not the kidney, while anorexia-induced lipolysis promoted late triglyceride and free fatty acid accumulation in both organs. These findings provide evidence for both direct and indirect regulation of peripheral metabolism by ER stress

Tissue Distribution, Metabolism, and Excretion of 3,3′-Dichloro-4′-sulfooxy-biphenyl in the Rat

Polychlorinated biphenyls (PCBs) with less chlorine atoms exhibit a greater susceptibility to metabolism than their more-chlorinated counterparts. Following initial hydroxylation of these less-chlorinated PCBs, metabolic sulfation to form PCB sulfates is increasingly recognized as an important component of their toxicology. Because procedures for the quantitative analysis of PCB sulfates in tissue samples have not been previously available, we have now developed an efficient, LC-ESI-MS/MS-based protocol for the quantitative analysis of 4-PCB 11 sulfate in biological samples. This procedure was used to determine the distribution of 4-PCB 11 sulfate in liver, kidney, lung, and brain as well as its excretion profile following its intravenous administration to male Sprague–Dawley rats. Following initial uptake of 4-PCB 11 sulfate, its concentration in these tissues and serum declined within the first hour following injection. Although biliary secretion was detected, analysis of 24 h collections of urine and feces revealed recovery of less than 4% of the administered 4-PCB 11 sulfate. High-resolution LC-MS analysis of bile, urine, and feces showed metabolic products derived from 4-PCB 11 sulfate. Thus, 4-PCB 11 sulfate at this dose was not directly excreted in the urine but was instead redistributed to tissues and/or subjected to further metabolism