Kathy Cassity Interview 2017

In this interview, Dr. Cassity discusses how she ended up at Western Oregon University, what she has done in her short time here, and what her plans are for her future here

Extension 3.0: Managing Agricultural Knowledge Systems in the Network Age

This paper develops the idea of “Extension 3.0” as an approach to agricultural extension that capitalizes on the network structure of local agricultural knowledge systems. Over the last century, agricultural knowledge systems have evolved into networks of widely distributed actors with a diversity of specializations and expertise. Agricultural extension programs need to manage these networks in ways that maximize the synergy between experiential, technical, and social learning. Using empirical research from California farmers, we highlight the structure of these networks within and across contexts, and the importance of boundary-spanning relationships. We provide some initial recommendations about actions needed to realize the goal of Extension 3.0, which is to deliver relevant agricultural knowledge to the right people, at the right time and plac

Flt3L controls the development of radiosensitive dendritic cells in the meninges and choroid plexus of the steady-state mouse brain

Antigen-presenting cells in the disease-free brain have been identified primarily by expression of antigens such as CD11b, CD11c, and MHC II, which can be shared by dendritic cells (DCs), microglia, and monocytes. In this study, starting with the criterion of Flt3 (FMS-like receptor tyrosine kinase 3)-dependent development, we characterize the features of authentic DCs within the meninges and choroid plexus in healthy mouse brains. Analyses of morphology, gene expression, and antigen-presenting function established a close relationship between meningeal and choroid plexus DCs (m/chDCs) and spleen DCs. DCs in both sites shared an intrinsic requirement for Flt3 ligand. Microarrays revealed differences in expression of transcripts encoding surface molecules, transcription factors, pattern recognition receptors, and other genes in m/chDCs compared with monocytes and microglia. Migrating pre-DC progenitors from bone marrow gave rise to m/chDCs that had a 5-7-d half-life. In contrast to microglia, DCs actively present self-antigens and stimulate T cells. Therefore, the meninges and choroid plexus of a steady-state brain contain DCs that derive from local precursors and exhibit a differentiation and antigen-presenting program similar to spleen DCs and distinct from microglia

Microarray Dataset of Transient and Permanent DNA Methylation Changes in HeLa Cells Undergoing Inorganic Arsenic-Mediated Epithelial-to-Mesenchymal Transition

The novel dataset presented here represents the results of the changing pattern of DNA methylation profiles in HeLa cells exposed to chronic low dose (0.5 µM) sodium arsenite, resulting in epithelial-to-mesenchymal transition, as well as DNA methylation patterns in cells where inorganic arsenic has been removed. Inorganic arsenic is a known carcinogen, though not mutagenic. Several mechanisms have been proposed as to how inorganic arsenic drives carcinogenesis such as regulation of the cell׳s redox potential and/or epigenetics. In fact, there are gene specific studies and limited genome-wide studies that have implicated epigenetic factors such as DNA methylation in inorganic arsenic-mediated epithelial-to-mesenchymal transition (EMT). However, genome-wide studies about the impact of 1) chronic, low-dose inorganic arsenic exposure on DNA methylation patterns during inorganic arsenic-induced epithelial-to-mesenchymal transition, and 2) the removal inorganic arsenic (reversal) on DNA methylation patterns, is lacking. For this dataset, two replicates were performed with each of the samples – non-treated, inorganic arsenic-treated, and reverse-treated cells. We provide normalized and processed data, and log2 fold change in DNA methylation. The raw microarray data are available through NCBI GEO, accession number GSE95232 and a related research paper has been accepted for published in Toxicology and Applied Pharmacology (Eckstein et al., 2017) [1]

Transient and Permanent Changes in DNA Methylation Patterns in Inorganic Arsenic-Mediated Epithelial-to-Mesenchymal Transition

Chronic low dose inorganic arsenic exposure causes cells to take on an epithelial-to-mesenchymal phenotype, which is a crucial process in carcinogenesis. Inorganic arsenic is not a mutagen and thus epigenetic alterations have been implicated in this process. Indeed, during the epithelial-to-mesenchymal transition, morphologic changes to cells correlate with changes in chromatin structure and gene expression, ultimately driving this process. However, studies on the effects of inorganic arsenic exposure/withdrawal on the epithelial-to-mesenchymal transition and the impact of epigenetic alterations in this process are limited. In this study we used high-resolution microarray analysis to measure the changes in DNA methylation in cells undergoing inorganic arsenic-induced epithelial-to-mesenchymal transition, and on the reversal of this process, after removal of the inorganic arsenic exposure. We found that cells exposed to chronic, low-dose inorganic arsenic exposure showed 30,530 sites were differentially methylated, and with inorganic arsenic withdrawal several differential methylated sites were reversed, albeit not completely. Furthermore, these changes in DNA methylation mainly correlated with changes in gene expression at most sites tested but not at all. This study suggests that DNA methylation changes on gene expression are not clear-cut and provide a platform to begin to uncover the relationship between DNA methylation and gene expression, specifically within the context of inorganic arsenic treatment

THE DEVELOPMENT OF FERROCENE-MODIFIED LINEAR POLY(ETHYLENIMINE) REDOX POLYMERS AND THEIR APPLICATION IN AMPEROMETRIC GLUCOSE BIOSENSORS AND COMPARTMENT-LESS BIOFUEL CELLS

A series of redox polymers was synthesized by attaching various ferrocene derivatives to linear poly(ethylenimine) (LPEI). These polymers displayed a remarkable ability to shuttle electrons from the active site of the enzyme glucose oxidase (GOx) to the surface of an electrode.The first type of polymer which was studied consisted of LPEI modified with a ferrocenylmethyl group (Fc-C1-LPEI). A new, versatile method was developed for the synthesis of this polymer at any substitution percentage (between 1% and 100%). The electrochemistry of these polymers in solution was unique and they displayed a double-wave behavior under acidic conditions which could be used to estimate the degree of protonation on the polymer backbone. As biosensors, it was found that polymers with 20% substitution performed the best, but that between 10% and 25%, the performance did not vary much.Because the polymer designated as Fc-C1-LPEI was believed to be unstable under physiological conditions due to its proximity to the LPEI backbone, polymers with different spacer lengths between the ferrocene and the polymer backbone were synthesized (Fc-C6-LPEI and Fc-C3-LPEI). Increasing the distance between the ferrocene and the backbone was shown to increase the lifetime of biosensors made with Fc-C6-LPEI and Fc-C3-LPEI 10-fold over that of Fc-C1-LPEI. Sensors made with Fc-C6-LPEI had lower maximum current densities than those made with Fc-C3-LPEI, and it was determined that three carbons was the optimal spacer length for these redox polymers.Once the optimal spacer length was determined, a new polymer, FcMe2-C3-LPEI was synthesized using dimethylferrocene instead of ferrocene. It was shown that the added methyl groups on the ferrocene resulted in biosensors with increased electrochemical and operational stability. This polymer (along with Fc-C3-LPEI) was shown to produce current densities of ~ 2 mA/cm2 at 37o C, which made it an attractive candidate for use in a biofuel cell. Biofuel cells using Fc-C3-LPEI and FcMe2-C3-LPEI as anodic mediators were constructed and produced power densities of up to 56 µW/cm2 in a stationary mode and 146 µW/cm2 when a rotating biocathode was used. FcMe2-C3-LPEI was shown to be a superior bioanode material for biofuel cells due to its lower redox potential and higher stability.In order to increase the biofuel cell power density further (as well as make a more effective glucose biosensor), tetramethylferrocene-modified LPEI (FcMe4-C3-LPEI) was synthesized in order to create a redox polymer with more stability and a lower redox potential. The desired effect of lowering the redox potential was achieved, and stationary biofuel cells using FcMe4-C3-LPEI produced power densities of up to 70 µW/cm2. However, when a rotating cathode was used, the performance of biofuel cells using FcMe4-C3-LPEI was not significantly better than that of biofuel cells using FcMe2-C3-LPEI. This was due to the lower limiting current densities produced by the FcMe4-C3-LPEI bioanodes

Final Report: Investigation into the Loss of the H.L. Hunley

The H.L. Hunley carried out the first successful submarine attack in history. However after a successful attack, the submarine disappeared with little evidence has to how it happened. This report documents work on two ONR grants exploring the naval architecture of the submarine. This work was conducted to support high-fidelity underwater explosion modeling of the attack at NSWCCD (not discussed here), but also sheds new light on the final mission and circumstances of the vessel’s loss. The vessel’s hullform, weights, stability are all discussed, along with model test for the vessel’s resistance and potential flooding rates. While the investigation did not reach a firm conclusion the cause of the loss, the results further illuminate the operation of vessel and avenues for further technical study.Office of Naval Research, Code 331https://deepblue.lib.umich.edu/bitstream/2027.42/142864/1/2017-001_final_complete.pdfDescription of 2017-001_final_complete.pdf : Repor

Epigenomic Reprogramming in Inorganic Arsenic-Mediated Gene Expression Patterns During Carcinogenesis

Arsenic is a ubiquitous metalloid that is not mutagenic but is carcinogenic. The mechanism(s) by which arsenic causes cancer remain unknown. To date, several mechanisms have been proposed, including the arsenic-induced generation of reactive oxygen species (ROS). However, it is also becoming evident that inorganic arsenic (iAs) may exert its carcinogenic effects by changing the epigenome, and thereby modifying chromatin structure and dynamics. These epigenetic changes alter the accessibility of gene regulatory factors to DNA, resulting in specific changes in gene expression both at the levels of transcription initiation and gene splicing. In this review, we discuss recent literature reports describing epigenetic changes induced by iAs exposure and the possible epigenetic mechanisms underlying these changes