The DNA Landscape: Development and Application of a New Framework for Visual Communication about DNA

Learning molecular biology involves using visual representations to communicate ideas about largely unobservable biological processes and molecules. Genes and gene expression cannot be directly visualized, but students are expected to learn and understand these and related concepts. Theoretically, textbook illustrations should help learners master such concepts, but how are genes and other DNA-linked concepts illustrated for learners? We examined all DNA-related images found in 12 undergraduate biology textbooks to better understand what biology students encounter when learning concepts related to DNA. Our analysis revealed a wide array of DNA images that were used to design a new visual framework, the DNA Landscape, which we applied to more than 2000 images from com-mon introductory and advanced biology textbooks. All DNA illustrations could be placed on the landscape framework, but certain positions were more common than others. We mapped figures about “gene expression” and “meiosis” onto the landscape framework to explore how these challenging topics are illustrated for learners, aligning these outcomes with the research literature to showcase how the overuse of certain representations may hinder, instead of help, learning. The DNA Landscape is a tool to promote research on visual literacy and to guide new learning activities for molecular biology

Integrin-linked kinase in muscle is necessary for the development of insulin resistance in diet-induced obese mice

Diet-induced muscle insulin resistance is associated with expansion of extracellular matrix (ECM) components, such as collagens, and the expression of collagen-binding integrin, α2β1. Integrins transduce signals from ECM via their cytoplasmic domains, which bind to intracellular integrin-binding proteins. The integrin-linked kinase (ILK)-PINCH-parvin (IPP) complex interacts with the cytoplasmic domain of β-integrin subunits and is critical for integrin signaling. In this study we defined the role of ILK, a key component of the IPP complex, in diet-induced muscle insulin resistance. Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF) diet for 16 weeks. Body weight was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice. However, HF-fed ILK(lox/lox)HSAcre mice had improved muscle insulin sensitivity relative to HF-fed ILK(lox/lox) mice, as shown by increased rates of glucose infusion, glucose disappearance, and muscle glucose uptake during a hyperinsulinemic-euglycemic clamp. Improved muscle insulin action in the HF-fed ILK(lox/lox)HSAcre mice was associated with increased insulin-stimulated phosphorylation of Akt and increased muscle capillarization. These results suggest that ILK expression in muscle is a critical component of diet-induced insulin resistance, which possibly acts by impairing insulin signaling and insulin perfusion through capillaries

Relaxin treatment reverses insulin resistance in mice fed a high-fat diet

The endogenous hormone relaxin increases vascular reactivity and angiogenesis. We demonstrate that acute relaxin infusion in lean C57BL/6J mice enhances skeletal muscle perfusion and augments muscle glucose uptake during a hyperinsulinemic-euglycemic clamp. However, an acute effect was absent in mice fed a high-fat (HF) diet for 13 weeks. In contrast, mice fed an HF diet for 13 weeks and continuously treated with relaxin for the final 3 weeks of the diet exhibited decreased fasting blood glucose. Insulin-stimulated whole-body glucose disappearance and percent suppression of hepatic glucose production are corrected by chronic relaxin. The increase in peripheral glucose utilization is a result of augmented in vivo skeletal muscle glucose uptake. Relaxin intervention improves endothelial-dependent vascular reactivity and induces a two-fold proliferation in skeletal muscle capillarity. The metabolic effects of the treatment are not attributed to changes in myocellular insulin signaling. Relaxin intervention reverses the accumulation of collagen III in the liver and collagen III and collagen IV in the heart; this is induced by HF feeding. These studies show the potential of relaxin in the treatment of diet-induced insulin resistance and vascular dysfunction. Relaxin provides a novel therapeutic approach targeting the extramyocellular barriers to insulin action, which are critical to the pathogenesis of insulin resistance

Incorporating Wifi into Watkins Regional Park

Final project for LARC471: Capstone Studio: Community Design (Spring 2022). University of Maryland, College Park.The need for new approaches to ensure internet access that would bridge society's "digital divide" became evident when instruction shifted online during the COVID-19 pandemic. Project BRIDGE, a UMD project funded by the National Science Foundation, aims to bring free Wi-Fi to public parks while creating technology that could bridge the digital divide and provide internet access to individuals and communities who now struggle to get online. In this studio, students explored community needs by conducting a community engagement session in Watkins Regional Park and then proposing design solutions to accommodate Wi-Fi use in various areas of the park.Prince George's County Department of Parks and Recreatio

Integrin α1-null mice exhibit improved fatty liver when fed a high fat diet despite severe hepatic insulin resistance

Hepatic insulin resistance is associated with increased collagen. Integrin α1β1 is a collagen-binding receptor expressed on hepatocytes. Here, we show that expression of the α1 subunit is increased in hepatocytes isolated from high fat (HF)-fed mice. To determine whether the integrin α1 subunit protects against impairments in hepatic glucose metabolism, we analyzed glucose tolerance and insulin sensitivity in HF-fed integrin α1-null (itga1(−/−)) and wild-type (itga1(+/+)) littermates. Using the insulin clamp, we found that insulin-stimulated hepatic glucose production was suppressed by ∼50% in HF-fed itga1(+/+) mice. In contrast, it was not suppressed in HF-fed itga1(−/−) mice, indicating severe hepatic insulin resistance. This was associated with decreased hepatic insulin signaling in HF-fed itga1(−/−) mice. Interestingly, hepatic triglyceride and diglyceride contents were normalized to chow-fed levels in HF-fed itga1(−/−) mice. This indicates that hepatic steatosis is dissociated from insulin resistance in HF-fed itga1(−/−) mice. The decrease in hepatic lipid accumulation in HF-fed itga1(−/−) mice was associated with altered free fatty acid metabolism. These studies establish a role for integrin signaling in facilitating hepatic insulin action while promoting lipid accumulation in mice challenged with a HF diet