Along with the surge of white supremacy across the U.S. there has been an equally strong and more robust anti-racist/racial justice social movement. For white folx, widely publicized killings of young black men have awakened a collective populace to the injustices that communities of color experience and have been fully aware of for generations. Social Identity Theory suggests that individuals create and define their place in society by which groups they belong. It also suggests a divide between in-groups and out-groups, each with their own lived experiences of oppression. This project investigates how white anti-racist activists and activists of color come to know and understand structural systems of oppression. We utilize semi-structured interviews from seven white anti-racist activists and seven activists of color in the Puget Sound Region of the U.S. to identify the processes by which each group comes to understand systemic oppression and how they frame systemic oppression. Our findings suggest that people of color learn about these systems through personal experiences, whereas white activists see the experiences in these systems as a third party. Our research suggests that awareness and education about systemic oppression may indicate a pivotal point in which individuals decide to take action and become activists. We present findings along with theoretical and practical implications for anti-racist activism. 

The importance of understanding the inflammatory response in the lungs is underscored by the fact that pneumonia and influenza illnesses led to an estimated 12,000 deaths in the 2015-16 U.S. flu season. Our research investigates the expression and regulation of versican in response to lung infections, both viral and bacterial. Versican is a chondroitin sulfate proteoglycan present in the extracellular matrix; it is expressed in lungs during embryonic development, mostly absent during healthy adulthood, and re-expressed in instances of inflammatory lung injury or infection. We are interested in understanding the pathways that result in versican upregulation, as preliminary data suggest that versican can be either pro- or anti-inflammatory, depending on the type of cell it arises from. My research project investigates this differential regulation phenomenon - recently, I have incorporated chromatin immunoprecipitation (ChIP) of versican transcription in both viral-stimulated macrophages and lung fibroblasts to explore the epigenetic factors that control expression. ChIP allows us to establish and quantify interactions between proteins and DNA; in our case, we are interested in transcription factors that follow interferon beta signaling (IFNb), which has been shown by our lab to be a key mediator of versican expression. IFNb itself is a known anti-viral cytokine, suggesting that versican may also follow this response to viral infection. If we can determine which transcription factors, if any, lead to an increased response of versican, we will have identified a signaling pathway by which to manipulate versican expression. The ultimate goal of this work is to develop a lung inflammation therapy by driving production of versican in an anti-inflammatory state. Utilizing versican's power as an immunomodulatory molecule could be a new tool for fighting severe inflammation associated with respiratory illnesses.

Chronic stress induces the release of hormones and neuropeptides including dynorphin, which activates Kappa Opioid Receptors (KOR) to encode the anxiogenic components of the stress response. Previous studies have identified the specific dynorphin-KOR neurochemical signaling responses in the regions of the brain known for regulation of reward systems, and thus may be potential therapeutic targets for stress-related conditions such as depression, anxiety, and substance use disorders. Formally, cells containing dynorphin-KOR have been difficult to study due to technical limitations of the available reagents. However, the generation of new tools including mice expressing promotor-driven cre-recombinase (e.g. KOR-Cre and prodynorphin-Cre) have allowed cell-specific gene expression using Cre-dependent viral expression of fluorophores combined with in-situ staining. In this study, the reliability of a phospho-KOR antibody was tested. The specificity of the immunostaining was verified by administering a KOR agonist, U50,488, in wild-type animals or transgenic animals lacking the G protein-coupled receptor kinase 3 (GRK3), which phosphorylates the KOR. Additionally, wild-type mice with a pre-treatment of norBNI, a KOR antagonist, followed by U50 were also tested. Immunohistochemistry of animal brain tissue showed that the norBNI pre-treated, wild-type animals and GRK3 knock-out animals had lower KORp-IR fluorescence compared to their wild-type counterparts treated with U50,488, verifying that the KORp antibody was reliable. After verification, this KORp antibody was utilized to characterize the dynorphin-KOR circuitry in the mouse brain. To do so, an excitatory opsin was injected into the DR of pDyn-Cre mice with an optic fiber implant. The DR region was then optically stimulated with blue light and dynorphin-releasing projections into the ventral tegmental area were verified by measuring KORp fluorescence. This experiment details one specific dynorphin-KOR pathway in the mouse brain that was not previously studied, and future experiments will utilize this approach to map the extent of dynorphin/KOR localization within the reward circuitry.

Drug addiction is a highly prevalent disease with common potentiating risk factors including stress-exposure, anxiety, and depression. A number of brain regions have been linked to behaviors that drive drug seeking and abuse, however little is known about how these regions communicate to regulate those behaviors. Currently, instruments can be used to record neuronal activity in vivo, however these devices are typically only able to record from one brain region at a time and don’t allow for specificity of neuronal stimulation. In order to improve the understanding of how brain regions communicate to drive behavior, there is a need to develop a multiple-site in vivo recording device that can record broad excitation signals while allowing optical stimulation of specific subtypes of neurons. In order to fill this need, I designed a dual-site optic delivering electrode or optrode. This device is small enough to mount on a mouse’s skull to promote naturalistic behavior with the ability to record non-specific electrical signals from the brain regions of interest, as well as optically stimulate specific subtypes of neurons. I also designed a program to process and analyze the data recorded by the device. If this device is successful, it will improve our understanding of how brain regions communicate to drive addiction-associated behaviors which could lead to therapeutic solutions for the treatment of addiction.

The catalytic activity of many metals can be increased when the catalyst exists as tiny nanoclusters as opposed to large bulk-like metal particles. Thus materials, or supports, that facilitate the growth of nanoparticle catalysts are highly desired. Of these supports, the most widely used are metal-oxides. The growth of catalysts on these supports can be better understood by studying the chemical bonding at the metal-oxide interface. The Mallouk group has found a calcium niobate nanosheet, HCa₂Nb₃O₁₀, that when used as a support both resists and reverses the coalescence of metal-oxide or hydroxide nanoparticles on the surface. These nanosheets are of additional interest because they are smooth on the atomic scale, similar to single crystal surfaces, with a large ratio of terrace sites to edge sites. Here, calorimetric measurements of the adsorption energies of silver and copper vapor on oxide thin films composed of four layers of these nanosheets are directly measured using adsorption calorimetry in ultrahigh vacuum. The initial heat of adsorption of silver atoms was found to be ~112 kJ/mol which closely resembles the predicted density functional theory (DFT) values for silver monomers. The growth mode of silver was determined using a surface sensitive spectroscopy technique, low-energy He+ ion scattering spectroscopy (LEIS). The number density of silver particles, as estimated from the LEIS data, was found to be ~2.2x10¹⁰ particles/cm² at 1.7 monolayer silver coverage. This is much lower than the particle densities on other metal-oxide supports and is attributed to the lower density of step/nanosheet edges on this support. The evolution of the LEIS signal indicates that silver grew as 3D nanoparticles. This data encourages further investigations of the adsorption calorimetry of different metals on this interesting support.

Irreversible damage to organs due to various illnesses that impacts millions of people daily are derived from a common problem: a lack of oxygen. This includes myocardial infarctions that reduce oxygen to the heart and lead to extensive tissue damage. Stem cell-derived cardiomyocytes have been used for direct injection into the heart after an infarct to increase muscle regeneration, but the survival rate and engraftment of these cells are found to be only five to ten percent due to the ischemic conditions. This project aims to increase cardiac regeneration after myocardial infarction through the development of photosynthetic stromal cells that can be injected alongside the stem cell-derived cardiomyocytes. Our initial research has been focused on combining mammalian cells with chloroplasts. We isolated chloroplasts from spinach and measured their oxygen output to demonstrate that chloroplasts produce oxygen. We have then successfully inserted the chloroplasts into mouse fibroblast by incubating them together in the presence of Epidermal Growth Factor as a proof of concept. Once the chloroplasts are successfully uptaken by stromal cells, their ability to produce oxygen upon light exposure will allow surrounding stem cell-derived cardiomyocytes to survive in ischemic conditions. Application of these cells would not be limited to cardiac regeneration, as they could be injected with other cell types into damaged tissues from ischemic conditions to increase oxygen and facilitate regeneration.