Utilization of an educational web based mobile app for acquisition and transfer of critical anatomical knowledge, thereby increasing classroom and laboratory preparedness in veterinary students

Contact time with students is becoming more valuable and must be utilized efficiently. Unfortunately, many students attend anatomy lectures and labs ill-prepared, and this limits efficiency. To address this issue we have created an interactive mobile app designed to facilitate the acquisition and transfer of critical anatomical knowledge in veterinary students, thereby increasing classroom and laboratory preparedness. We have found that in contrast to a traditional reading assignment, utilization of such an app to introduce students to a subject area significantly enhanced the initial learning of anatomy and the transfer of that learned material to a related, but novel area. We propose that students using the apps were subsequently better prepared for lecture and lab, than students using the more traditional method of reading a textbook. Exposure of students to a topic prior to lecture and laboratory, using methods that students embrace, can only lead to a more efficient and better educational experience

Western Guide to Working with Teaching Assistants

This guide offers valuable strategies for working effectively with both tutorial and laboratory TAs, preparing TAs for grading, managing TA teams, mentoring TAs as junior instructors, and more.https://ir.lib.uwo.ca/tsc-purple-guides/1000/thumbnail.jp

Optimization of Ectopic Gene Expression in Skeletal Muscle Through DNA Transfer by Electroporation.

Background Electroporation (EP) is a widely used non-viral gene transfer method. We have attempted to develop an exact protocol to maximize DNA expression while minimizing tissue damage following EP of skeletal muscle in vivo. Specifically, we investigated the effects of varying injection techniques, electrode surface geometry, and plasmid mediums. Results We found that as the amount of damage increased in skeletal muscle in response to EP, the level of β-galactosidase (β-gal) expression drastically decreased and that there was no evidence of β-gal expression in damaged fibers. Two specific types of electrodes yielded the greatest amount of expression. We also discovered that DNA uptake in skeletal muscle following intra-arterial injection of DNA was significantly enhanced by EP. Finally, we found that DMSO and LipoFECTAMINE™, common enhancers of DNA electroporation in vitro, had no positive effect on DNA electroporationin vivo. Conclusions When injecting DNA intramuscularly, a flat plate electrode without any plasmid enhancers is the best method to achieve high levels of gene expression

The mERG1a channel modulates skeletal muscle MuRF1, but not MAFbx, expression.

INTRODUCTION: We investigated the mechanism by which the MERG1a K+ channel increases ubiquitin proteasome proteolysis (UPP). METHODS: Hindlimb suspension and electro-transfer of Merg1a cDNA into mouse gastrocnemius muscles induced atrophy. RESULTS: Atrophic gastrocnemius muscles of hindlimb-suspended mice express Merg1a, Murf1, and Mafbx genes. Electrotransfer of Merg1a significantly decreases muscle fiber size (12.6%) and increases UPP E3 ligase Murf1 mRNA (2.1-fold) and protein (23.7%), but does not affect Mafbx E3 ligase expression. Neither Merg1a-induced decreased fiber size nor Merg1a-induced increased Murf1 expression is curtailed significantly by coexpression of inactive HR-Foxo3a, a gene encoding a transcription factor known to induce Mafbx expression. CONCLUSIONS: The MERG1a K+ channel significantly increases expression of Murf1, but not Mafbx. We explored this expression pattern by expressing inactive Foxo3a and showing that it is not involved in MERG1a-mediated expression of Murf1. These findings suggest that MERG1a may not modulate Murf1 expression through the AKT/FOXO pathway

Rectangular Symmetry Morphologies in a Topographically Templated Block Copolymer

Using an array of majority-block-functionalized posts makes it possible to locally control the self-assembly of a block copolymer and achieve several morphologies on a single substrate. A template consisting of a square symmetry array of posts produces a square-symmetry lattice of microdomains, which doubles the areal density of features.Semiconductor Research CorporationFENA CenterSemiconductor Research Corporation. Nanoscale Research InitiativeSingapore-MIT AllianceNational Science Foundation (U.S.)Taiwan Semiconductor Manufacturing CompanyTokyo Electron LimitedNational University of Singapor

Influences on Cookware Choices of Young Adults

This article was originally published in the Undergraduate Research Journal for the Human Sciences.This study employed a focus group of thirteen mid-western university students ages 20-25 to test the hypothesis that after observing a demonstration using high-end stainless steel cookware, college student participants would exhibit a greater propensity to purchase the cookware than prior to the session. Questions regarding cookware choices were asked before and after the guided demonstration. Results confirmed that a guided demonstration of high-end, stainless steel cookware increased the likelihood of future purchase.This project was supported by a Special Emphasis Grant for undergraduate student/faculty collaborative research from Bradley University and by the Healthy Gourmet Cookware Compan

An epigenetic switch regulates the ontogeny of AXL-positive/EGFR-TKi-resistant cells by modulating miR-335 expression.

Despite current advancements in research and therapeutics, lung cancer remains the leading cause of cancer-related mortality worldwide. This is mainly due to the resistance that patients develop against chemotherapeutic agents over the course of treatment. In the context of non-small cell lung cancers (NSCLC) harboring EGFR-oncogenic mutations, augmented levels of AXL and GAS6 have been found to drive resistance to EGFR tyrosine kinase inhibitors such as Erlotinib and Osimertinib in certain tumors with mesenchymal-like features. By studying the ontogeny of AXL-positive cells, we have identified a novel non-genetic mechanism of drug resistance based on cell-state transition. We demonstrate that AXL-positive cells are already present as a subpopulation of cancer cells in Erlotinib-naïve tumors and tumor-derived cell lines and that the expression of AXL is regulated through a stochastic mechanism centered on the epigenetic regulation of miR-335. The existence of a cell-intrinsic program through which AXL-positive/Erlotinib-resistant cells emerge infers the need of treating tumors harboring EGFR-oncogenic mutations upfront with combinatorial treatments targeting both AXL-negative and AXL-positive cancer cells