Increased racial tensions in America should be considered in evaluating current psychotherapeutic and social structures. Functional Analytic Psychotherapy (FAP) argues that divulging vulnerable information about oneself is essential for emotional intimacy. When vulnerability is responded to with attempts to build safety, vulnerable behavior is reinforced (strengthened). This reciprocal process of vulnerability and building safety aids in the development of intimate relationships across social and psychotherapeutic settings. The interaction model of FAP has never been examined through an interracial lens. In interracial interactions, people may be less comfortable being vulnerable, which may contribute to increased social anxiety. These communication differences may partially explain lower rates of efficacy in cross-cultural psychotherapy. Our study analyzed the effect of race on vulnerability and anxiety as important elements in the well-established model of intimate relationship development. During same-race and interracial mock therapeutic interactions, undergraduate participants (representing clients) were asked questions intended to elicit vulnerability by research assistants. Heart rate (HR) data were recorded from participants as a physiological measure of anxiety throughout the interaction. Participant vulnerability was assessed through self-report and behavioral coding by blind, independent research assistants. We hypothesize that participants in the interracial interactions will show higher levels of anxiety, as measured by HR data, and lower levels of vulnerability, as measured by self report and behavioral coding, compared to participants in same-race interactions. This project may reveal that developing organic interracial connections is more difficult than developing same-race connections. This would indicate a need to modify current social and psychotherapeutic structures to facilitate the creation of effective and meaningful interracial relationships.

Stroke is the leading cause of long-term disability in the USA. Ischemic preconditioning (IPC) is a neuroprotective phenomenon wherein a brief ischemic exposure induces robust neuroprotection against subsequent prolonged ischemia. The Weinstein laboratory has previously demonstrated: (i) a robust type 1 interferon response in cortical microglia following IPC, (ii) type I interferon signaling in microglia is required for IPC-mediated protection and (iii) IPC induces a robust increase in the number of microglia in preconditioned cortex. An initial component of my project was to validate this microglial response by first staining for Iba1 (a microglial marker) alone and then double staining for Iba1 and proliferation marker BrdU. We used immunofluorescent microscopy (IFM) following by quantitative stereology (QS). Our hypothesis was that type I interferon signaling is necessary for IPC-induced microglial proliferation. We carried out IPC on WT and type 1 interferon receptor deficient (IFNAR-/-) mice and quantified cortical microglial number and proliferation as above. Preliminary results were: (i) in naïve WT, 0.643 ± 0.038 (mean ± S.D), Iba1+ cells per position, (ii) in preconditioned WT, 1.113 ± 0.1385, (iii) in naïve IFNAR1-/-, 0.751 ± 0.058 and in preconditioned IFNAR1-/-, 0.903 ± 0.125. Two way ANOVA revealed a significant difference between naïve and IPC-induced cortical microglia numbers [F(1,14)=9.62, p=0.0078], but no significant effect of genotype [F(1,14)=0.258, p=0.619]. IPC induced increases in the number of cortical Iba1+/BrdU+ proliferating microglia in both IFNAR1-/- (0.451 ± 0.107) and WT (0.205 ± 0.069) mice. These results suggest a complex picture in which deficiency in type 1 IFN signaling may not influence IPC-induced microglial proliferation but does attenuate the overall number of cortical microglia. This raises the possibility that type 1 IFN signaling may be required for optimal microglial survival following IPC. More studies will be required to confirm the above findings and explore possible mechanisms.

36.7 million people worldwide are living with HIV/AIDS, of which almost 15 million receive antiretroviral therapy (ART). These patients require regular HIV-1 viral load (VL) tests to monitor ART effectiveness and compliance. However, the majority of affected people live in low-resource settings where disease monitoring through medical laboratory-based systems, such as nucleic acid amplification tests (NAATs), are inaccessible. There is an increasing need for accurate, affordable HIV-1 VL tests at the point-of-care (POC). We previously demonstrated the ability to leverage an electrokinetic separation and preconcentration technique, isotachophoresis (ITP), and an isothermal nucleic acid amplification method to develop a proof-of-concept POC NAAT for extraction, amplification, and detection of nucleic acids from human serum. The limit of detection (LoD) of our paper-based test was hampered by the loss of nucleic acids during ITP across the paper membrane. This work is focused on lowering the LoD of our test by improving the isotachophoretic extraction of nucleic acids from human serum. We have addressed the adsorption of nucleic acids by screening membrane types and pre-treatment methods. We have observed significant nucleic acid entanglement of DNA greater than 50,000 base pairs in length, which we can mitigate using DNA shearing techniques. We have also developed specialized ITP chemsitries for increased extraction efficiency. The completion of this work will result in more effective separation and purification of nucleic acids from human serum, ultimately leading to a reduction of target loss and improved test sensitivity. Employing the ITP extraction techniques developed in this work will aid our lab's ongoing efforts to create a POC NAAT for monitoring HIV-1 viral load.

Color blindness is defined as a perspective understanding one’s racial identity is irrelevant and it is best to ignore the importance of race and skin color. This ideology is embraced by whites who deny their prejudice through this modern form of racism by diminishing other’s race and culture and claiming to view all people as equal. Although white people may believe their intentions behind color blindness are good by not judging people by the color of their skin, but rather by the content of their character, alternately the true motivation behind the color blindness ideology may be white people’s discomfort around black people, which causes them to avoid color all together. We believe that color blindness is a modern form of racism in which individuals suppress their discomfort among blacks. Therefore, we predict higher levels of color-blindness will correlate with lower levels of allophilia, which represents positive attitudes, feelings, and demeanor towards minorities. We tested this prediction in a survey study in which UW undergraduate students completed measures of color-blindness and allophilia towards Black people. The current study also seeks to investigate how social desirability influences this relationship between color blindness and allophilia. Social desirability is a biased response in which the respondent answers the survey question in a way that would be generally accepted and favored by society rather than being truthful. We hypothesize that if we account for social desirability, the correlation between color blindness and allophilia will be stronger because we predict that social desirability masks the real relationship between the two variables. Thus, people with higher social desirability will be more untruthful, resulting in a higher score of allophilia, when in reality their allophilia score should be lower. Our study explores the relationship between color blindness and allophilia and the role in which social desirability plays.

Organic materials show promise as alternative materials for many modern-day electronics applications, such as transistors, LEDs, and photovoltaics. They hold many advantages over their inorganic counterparts, such as being lighter weight, lower cost, and flexible. Self-healing polymers are a specific form of organic polymer that are particularly promising because of their potential use in flexible devices. Self-healing materials have the capacity to spontaneously reform damaged bonds, thereby returning the material to its original state and recovering its initial properties. Imine bonds are a type of self-healing bond. Imines have a highly dynamic nature, allowing for the reshuffling of bonds required to recover material properties. Much research has been done on the use of imine bonds in self-healing polymers; however, no work has been done utilizing imine bonds for self-healing in semiconducting polymers. To incorporate self-healing behavior into a semiconducting polymer, we have investigated the synthesis of a poly(azomethine), a semiconducting polymer with an imine bond along the backbone. Initially, as a proof-of-concept for the dynamic exchange of bonds in our specific system, we reacted aniline with 2-thiophenealdehyde to form an imine. Then, to determine if bond exchange occurred, the imine produced was reacted with another amine. The reaction showed that a significant amount of imine exchanged, so we moved on to a polymer system. We synthesized 4,4'-dinitrotriphenylamine, which we then reduced to produce a diamine species. This diamine was then polymerized with a dialdehyde species, resulting in a fully conjugated polymer with multiple imine bonds along the backbone. The polymer will be made into thin films for testing. Mechanical properties will be investigated to determine initial film properties. Additionally, transistors will be produced to see if electrical properties can be recovered after the film has been damaged.

Current drug testing methods are unable to accurately predict and study the effects of drugs on human myocardial tissue. These methods are unable to accurately mimic the physiology and maturity of native cardiac tissue, and as a result, the tissues are unable to react to cardiotoxic drugs the same way that native cardiac tissue. Therefore, there is a need for physiologically accurate and mature tissue constructs in order to test clinical drugs for effectiveness, cardiotoxicity, and arrhythmic effects. To fulfill this need, we will use an electroconductive bioink containing decellularized extracellular matrix (dECM) from porcine cardiac tissue, reduced graphene oxide (rGO), and incorporated human induced-pluripotent stem cell (hiPSC)-derived cardiomyocytes to develop a more physiologically accurate cardiac tissue construct. This will result in more adequate cell maturation, and therefore, more accurate preclinical drug screening. The success of this project would lead to the development of high throughput production of biomimetic cardiac tissue models for use in accurate drug screening, along with improving the understanding of cardiac maturation.

Nuclear coercion rests on the threat of force to compel a demand. Some strategists contend that nuclear coercion does not work between nuclear adversaries. The theory of the nuclear revolution posits that military victory is not possible in the nuclear era, and therefore military power cannot advance political ends. Others maintain that nuclear coercion is indeed possible, and the nuclear balance of power between adversaries shapes political outcomes. This study explores whether strategic superiority generates coercive leverage in crisis bargaining. It employs a qualitative case study analysis of Soviet decision making during the Cuban Missile Crisis to test rival theories of nuclear strategy.

Plasma, the fourth state of matter, is created by introducing a gas - in this case, helium - to an electric field. This field ionizes the helium atoms, which in turn ionize other molecules, creating a wide variety of highly reactive species. Previous work at Edmonds Community College demonstrated the efficacy of an atmospheric pressure plasma jet (APPJ) in killing endospores of Bacillus atrophaeus for the purpose of spacecraft sterilization for NASA (Bernard et al., 2017). With increasing rates of antibiotic resistance, there is interest in using an APPJ in healthcare settings to eliminate harmful pathogens and therefore promote wound healing. However, given its destruction of endospores, it is unclear if the APPJ would damage living tissue. The purpose of this research was to analyze the effect of an APPJ on multicellular eukaryotic organisms. The impact of different exposure times of the APPJ upon both germinated and ungerminated Zinnia elegans seeds, and the effects on plant growth, was studied. The optimal exposure time for germinated seeds was between one and two minutes, while treatments greater than 2 minutes may increase germination rate.

Atherosclerotic vascular disease and its resulting myocardial infarction (MI) is the leading cause of death in subjects with diabetes. Additionally, patients with a history of a MI are more likely to experience a recurrent MI, however the mechanism is not yet understood. Previous work from our laboratory, and others, has demonstrated that diabetes accelerates atherosclerosis partly by affecting monocytes and macrophages, resulting in increased inflammation and macrophage accumulation in the artery wall. Work from others has shown that experimental MI can also accelerate atherosclerosis in non-diabetic mice by increasing the number of blood monocytes, which enter the artery wall to become inflammatory macrophages. Thus, we wanted to ask if diabetes and experimental MI have synergistic effects on macrophage accumulation in the artery wall. Experimental MI, or sham surgeries, were carried out in an atherosclerotic-prone, transgenic mouse model of type 1 diabetes that relies on viral mimicry (Ldlr-/-Gp+) and in non-diabetic controls. At the end of the study, cross sections of the dissected brachiocephalic artery were used to quantify macrophage accumulation by measuring areas of Mac-2 immunoreactivity on sections adjacent to the largest cross-sectional lesion. If macrophage accumulation is synergistically increased with diabetes and experimental MI, attempts will be made to understand the underlying mechanism. Atherosclerotic macrophage accumulation is a dynamic process that involves monocyte recruitment and local proliferation. Macrophage proliferation and monocyte recruitment will be analyzed by staining with proliferation marker Ki67 and estimating the number of previously labeled monocytes that enter the atherosclerotic lesion, respectively. To mechanistically test the role of monocyte recruitment on macrophage accumulation, Mac-2 staining will be quantified in mice (diabetic and non-diabetic with and without MI) deficient in a key adhesion molecule (CD49D) required for monocyte adhesion to activated endothelium. These results should yield important information on potential synergistic effects of diabetes and MI.

 In the United States, Major Depressive Disorder and Generalized Anxiety Disorder are among the most prevalent of mental health disorders. There are, however, disparities in the prevalence of depression and anxiety between racial and ethnic groups. Generally, whites have higher rates of depression and anxiety than blacks, but blacks have a higher rate of persistent depression than whites. One potential factor relevant to this disparity in depression and anxiety rates is ethnic identity. This study therefore sought to investigate how ethnic identity predicts depression and anxiety differentially between blacks and whites. Based on past literature, we hypothesized that higher ethnic identity would predict lower depression and anxiety in blacks, in that having a strong black identity would inoculate individuals from the harmful and depressogenic effects of discrimination, a known risk for depression in blacks. We hypothesized that ethnic identity would have no effect in whites. The study recruited black (n=54) and white (n=64) participants from Amazon Mechanical Turk to complete a battery of self-report questionnaires including measures of ethnic identity, depression, and anxiety. A linear regression analysis was computed predicting depression and anxiety from measures of ethnic identity, with race as a moderator variable. Results indicated that higher ethnic identity had no significant effect on depression and anxiety in whites, but predicted higher depression and anxiety in blacks. Therefore our hypothesis was not supported. These data contradict previous findings that strong ethnic identity can be a protective factor against depression and anxiety. It is possible that, in today’s political climate of increased white nationalism and violence against blacks, ethnic identity may in fact be becoming a risk factor. Future studies would explore how ethnic identity corresponds to heightened sensitivity to discrimination, thereby predicting higher depression and anxiety in blacks.