Augmented Reality in the Classroom

Low vision can have an exceptionally negative impact on a student’s ability to learn, especially when subjected to the conventional education system. In this environment, students are expected to adhere to a lecture that delivers most information visually via a whiteboard or a projector screen. The goal of this project is to create a customizable application for a smartphone that implements selective processing in order to make it easier for visually impaired students to engage with and learn from lectures. Specifically, this application is written in the Java language for the Android platform. The application uses OpenGL ES, a C-like language for the mobile platform, in order to perform image processing. Filters written in OpenGL ES are used to modify the image read by the phone’s camera. Using these filters, the application can modify an image by stretching, magnifying, and enhancing the color and contrast. The specific processes included in the application include Sobel Edge Detection, Dilation, Zoom and Contrast. Hardware acceleration is also performed using OpenGL ES. A direct consequence of this project is solving a problem in the classroom for visually impaired students not yet addressed by current technologies. While this project needs further development to substantially help students with severe peripheral vision, it was successful in implementing the desired augmentation and can serve as a foundation for future usability improvements

Feasibility of a Transient Dynamic Design Analysis Method

This article addresses the degree of success that may be achieved by using simple equipment–vehicle models that produce time history responses whose equipment fixed base modal maximum response values are equivalent to those found in the U.S. Navy's dynamic design analysis method. The criteria of success is measured by a comparison of the results with typical interim shock design values. The equipment models reported are limited to two- degree and three degrees of freedom systems; the model of the vehicle to which the equipment is attached consists solely of a rigid mass and an elastic spring; and the shock excitation is produced by an ideal impulse that is applied to the vehicle mass

Peroxiredoxin 3 levels regulate a mitochondrial redox setpoint in malignant mesothelioma cells

Peroxiredoxin 3 (PRX3), a typical 2-Cys peroxiredoxin located exclusively in the mitochondrial matrix, is the principal peroxidase responsible for metabolizing mitochondrial hydrogen peroxide, a byproduct of cellular respiration originating from the mitochondrial electron transport chain. Mitochondrial oxidants are produced in excess in cancer cells due to oncogenic transformation and metabolic reorganization, and signals through FOXM1 and other redox-responsive factors to support a hyper-proliferative state. Over-expression of PRX3 in cancer cells has been shown to counteract oncogene-induced senescence and support tumor cell growth and survival making PRX3 a credible therapeutic target. Using malignant mesothelioma (MM) cells stably expressing shRNAs to PRX3 we show that decreased expression of PRX3 alters mitochondrial structure, function and cell cycle kinetics. As compared to control cells, knockdown of PRX3 expression increased mitochondrial membrane potential, basal ATP production, oxygen consumption and extracellular acidification rates. shPRX3 MM cells failed to progress through the cell cycle compared to wild type controls, with increased numbers of cells in G2/M phase. Diminished PRX3 expression also induced mitochondrial hyperfusion similar to the DRP1 inhibitor mdivi-1. Cell cycle progression and changes in mitochondrial networking were rescued by transient expression of either catalase or mitochondrial-targeted catalase, indicating high levels of hydrogen peroxide contribute to perturbations in mitochondrial structure and function in shPRX3 MM cells. Our results indicate that PRX3 levels establish a redox set point that permits MM cells to thrive in response to increased levels of mROS, and that perturbing the redox status governed by PRX3 impairs proliferation by altering cell cycle-dependent dynamics between mitochondrial networking and energy metabolism