Textbook Remix: An Introduction to LibreTexts for OER Editing

So, you’ve found an open textbook that you really like, but it’s not quite right for your class? LibreTexts might be the answer! Join us for this informal webinar to learn a little more about this online platform designed for customizing and distributing open textbooks. From Gettysburg College, Scholarly Communications Librarian Mary Elmquist will provide an introduction to the platform, its structure and features, and Dr. Alice Brawley Newlin, Assistant Professor of Management, will speak on her ongoing experiences using LibreTexts to edit and implement an open textbook for a Statistical Methods course. This session should provide insight for both instructors interested in LibreTexts for their own projects and for librarians and other staff on campus who work to support OER adoption. Please bring your questions, as there will be plenty of time for Q&A

Faculty and Student Perspectives on Open Education at Gettysburg College

Commercially available textbooks and course materials are often expensive for students and sometimes don’t cover topics in exactly the way you might prefer to teach. Freely available and completely adaptable open educational resources (OER) have risen in popularity in recent years, both nationwide and locally, as a way to address both issues. Join us to hear from Alice Brawley Newlin (Management), Tasha Gownaris (Environmental Studies), Chris Oechler (Spanish), and Ryan Nedrow ’22 to hear about their experiences with OER in the classroom. Panelists will talk honestly about the benefits, drawbacks, challenges, and successes associated with open course materials in order to give you a better sense of whether OER might be a good fit in your own context

A system for exposing molecules and cells to biologically relevant and accurately controlled steady-state concentrations of nitric oxide and oxygen

Nitric oxide (NO) plays key roles in cell signaling and physiology, with diverse functions mediated by NO concentrations varying over three orders-of-magnitude. In spite of this critical concentration dependence, current approaches to NO delivery in vitro result in biologically irrelevant and poorly controlled levels, with hyperoxic conditions imposed by ambient air. To solve these problems, we developed a system for controlled delivery of NO and O[subscript 2] over large concentration ranges to mimic biological conditions. Here we describe the fabrication, operation and calibration of the delivery system. We then describe applications for delivery of NO and O[subscript 2] into cell culture media, with a comparison of experimental results and predictions from mass transfer models that predict the steady-state levels of various NO-derived reactive species. We also determined that components of culture media do not affect the steady-state levels of NO or O[subscript 2] in the device. This system provides critical control of NO delivery for in vitro models of NO biology and chemistry.National Cancer Institute (U.S.) (CA026731)National Cancer Institute (U.S.) (CA116318)National Institute of Environmental Health Sciences (ES002109

10 Years of C-K Theory: A Survey on the Academic and Industrial Impacts of a Design Theory.

The goal of our research1 was to understand what is expected today from a design theory and what types of impact such type of scientific proposition may reach. To answer these questions with a grounded approach we chosed to study the developement of C-K theory as phenomenon per se that can inform our research work. C-K theory is clearly recognized as a design theory and it is a good representative of the level of generality and abstraction of contemporary design theory. Indeed, the validity of the theory as such has already been documented (e.g. Hatchuel & Weil 2002, 2003, 2008, 2009; Kazakçi 2009; Reich et al 2010; Le Masson et al 2010; Ullah et al 2012). Instead the current work sets out to understand the dissemination and the impact of the theory in both academic and industrial fields. The data collection overlooks the literature on C-K theory in English and in French, and includes interviews and feedbacks of students and industrial partners who applied C-K methodologies and tools. This research confirms the rapid diffusion and multiples impact of C-K theory. Beyond, such study signals that there are important expectations and potential impacts of a Design Theory within the field of knowledge at large. However there are strong conditions to meet these expectations: generality, generativity, and relatedness to contemporary sciences. A similar research could be done on Nam Suh's axiomatic approach to further test these conditions. It is impossible to say what will be the next generations of Design theory but it is sure that they should progress on these directions

Transgenic amplification of glucocorticoid action in adipose tissue causes high blood pressure in mice

Obesity is closely associated with the metabolic syndrome, a combination of disorders including insulin resistance, diabetes, dyslipidemia, and hypertension. A role for local glucocorticoid reamplification in obesity and the metabolic syndrome has been suggested. The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) regenerates active cortisol from inactive 11-keto forms, and aP2-HSD1 mice with relative transgenic overexpression of this enzyme in fat cells develop visceral obesity with insulin resistance and dyslipidemia. Here we report that aP2-HSD1 mice also have high arterial blood pressure (BP). The mice have increased sensitivity to dietary salt and increased plasma levels of angiotensinogen, angiotensin II, and aldosterone. This hypertension is abolished by selective angiotensin II receptor AT-1 antagonist at a low dose that does not affect BP in non-Tg littermates. These findings suggest that activation of the circulating renin-angiotensin system (RAS) develops in aP2-HSD1 mice. The long-term hypertension is further reflected by an appreciable hypertrophy and hyperplasia of the distal tubule epithelium of the nephron, resembling salt-sensitive or angiotensin II–mediated hypertension. Taken together, our findings suggest that overexpression of 11β-HSD1 in fat is sufficient to cause salt-sensitive hypertension mediated by an activated RAS. The potential role of adipose 11β-HSD1 in mediating critical features of the metabolic syndrome extends beyond obesity and metabolic complications to include the most central cardiovascular feature of this disorder

Insufficiency of Janus Kinase 2–Autonomous Leptin Receptor Signals for Most Physiologic Leptin Actions

OBJECTIVE: Leptin acts via its receptor (LepRb) to signal the status of body energy stores. Leptin binding to LepRb initiates signaling by activating the associated Janus kinase 2 (Jak2) tyrosine kinase, which promotes the phosphorylation of tyrosine residues on the intracellular tail of LepRb. Two previously examined LepRb phosphorylation sites mediate several, but not all, aspects of leptin action, leading us to hypothesize that Jak2 signaling might contribute to leptin action independently of LepRb phosphorylation sites. We therefore determined the potential role in leptin action for signals that are activated by Jak2 independently of LepRb phosphorylation (Jak2-autonomous signals). RESEARCH DESIGN AND METHODS: We inserted sequences encoding a truncated LepRb mutant (LepRb$^{\Delta65c}$, which activates Jak2 normally, but is devoid of other LepRb intracellular sequences) into the mouse Lepr locus. We examined the leptin-regulated physiology of the resulting $\Delta/\Delta$ mice relative to LepRb-deficient $db/db$ animals. RESULTS: The $\Delta/\Delta$ animals were similar to $db/db$ animals in terms of energy homeostasis, neuroendocrine and immune function, and regulation of the hypothalamic arcuate nucleus, but demonstrated modest improvements in glucose homeostasis. CONCLUSIONS: The ability of Jak2-autonomous LepRb signals to modulate glucose homeostasis in $\Delta/\Delta$ animals suggests a role for these signals in leptin action. Because Jak2-autonomous LepRb signals fail to mediate most leptin action, however, signals from other LepRb intracellular sequences predominate

Impact of Sleep and Circadian Disruption on Energy Balance and Diabetes: A Summary of Workshop Discussions

A workshop was held at the National Institute for Diabetes and Digestive and Kidney Diseases with a focus on the impact of sleep and circadian disruption on energy balance and diabetes. The workshop identified a number of key principles for research in this area and a number of specific opportunities. Studies in this area would be facilitated by active collaboration between investigators in sleep/circadian research and investigators in metabolism/diabetes. There is a need to translate the elegant findings from basic research into improving the metabolic health of the American public. There is also a need for investigators studying the impact of sleep/circadian disruption in humans to move beyond measurements of insulin and glucose and conduct more in-depth phenotyping. There is also a need for the assessments of sleep and circadian rhythms as well as assessments for sleep-disordered breathing to be incorporated into all ongoing cohort studies related to diabetes risk. Studies in humans need to complement the elegant short-term laboratory-based human studies of simulated short sleep and shift work etc. with studies in subjects in the general population with these disorders. It is conceivable that chronic adaptations occur, and if so, the mechanisms by which they occur needs to be identified and understood. Particular areas of opportunity that are ready for translation are studies to address whether CPAP treatment of patients with pre-diabetes and obstructive sleep apnea (OSA) prevents or delays the onset of diabetes and whether temporal restricted feeding has the same impact on obesity rates in humans as it does in mice