Autistic Spectrum Disorder (ASD) is a heterogeneous disease characterized by varying degrees of social dysfunction. Several studies by the CDC show that 1 in 68 children in the United States are affected by ASD, this number could be 1 in 45 according to the newest studies by various government resources. So far pharmacological treatments are not effective in most cases, only treating a few symptoms at best rather than the whole. Several theories exist for the pathogenesis of ASD; however, much is still unknown despite multiple studies. Investigators often tend to research the pathology of ASD based primarily within their scientific discipline, and we feel this narrow view limits a deep understanding of the disorder. This literature review explores neurostructural, neurochemical, and genetic disciplines, synthesizing an overall hypothesis of the pathogenesis of the disease. Specifically, we explore specific groups of genes known to have a causal effect in ASD and focus on how they might interact to produce the disorder. We analyze these genes to see how they affect different neurotransmitter systems and impact different structures of the brain. We are restricting our database search using terms such as “genes”, “synaptic transmission”, “brain areas” and “homeostatic/compensatory mechanisms” associated with ASD. The literature suggests that genetic aberrations in ASD are quite numerous and cause cascading effects throughout the brain, affecting synaptic transmission in many regions. Our analysis suggests that ASD is a polygenetic disorder where numerous small changes in protein function occur in multiple brain regions. Homeostatic and compensatory mechanisms cannot correct these cellular and connectivity deficits, and ASD develops. We hope this review helps researchers take a broad view of the various genes, neurotransmitter systems, and anatomical structures implicated in ASD as they embark on future studies.
 

Human immunodeficiency virus (HIV) infects over one million women annually. Pre-exposure prophylaxis (PrEP) drugs are developed to prevent HIV acquisition and have yielded varying results in women. Despite adherence, recent evidence suggests biological factors, such as the vaginal microbiome, contributes to its variability. Such drugs are tenofovir (TFV), tenofovir alafenamide (TAF), tenofovir disoproxil fumarate (TDF), and dapivirine (DPV) and their efficacy in HIV prevention are vital to public health. There is recent evidence demonstrating vaginal dysbiosis is associated with an increased risk of HIV transmission by bacterial metabolism, altering PrEP pharmacokinetics (PK). Vaginal dysbiosis occurs when the dominant Lactobacillus is replaced with a more diverse anaerobic community, including Gardnerella. To investigate the impact of the vaginal microbiome on PrEP PK, I incubated target Jurkat cells, with various PrEP drugs in the presence of Lactobacillus and Gardnerella vaginalis. Lactobacillus spp. represents the healthy commensal species, while G. vaginalis represents dysbiosis. Abiotic and drug free samples were used as negative controls. Using Liquid Chromatography-tandem Mass Spectrometry, I measured residual PrEP drugs, bacteria mediated metabolites, and pharmacodynamically active metabolites representing target cell uptake at different time points. In the presence of G. vaginalis, we saw a significant decrease in extracellular TFV (p<0.0001) and DPV (p<0.001) when compared to Lactobacillus and abiotic controls. We saw a milder effect with TDF (p=0.004) and TAF (p=0.03), most likely due to the pro-drug formulation. When comparing bacterial metabolites, we observed an increase in the presence of G. vaginalis for TFV (p=0.0001), but not in abiotic and Lactobacillus samples. Similarly, we saw a decrease in pharmacodynamically active metabolites in the presence of G. vaginalis for TFV (p=0.0004) and DPV (p<0.0001) and an increase in abiotic and Lactobacillus samples. By improving the health of the vaginal microbial communities, we can improve the adherence of PrEP drugs and improve HIV prevention.

Human immunodeficiency virus (HIV) infections are often paired with microbial translocation within the gastrointestinal tract (GI). In-vivo studies show that HIV-associated microbial translocation results from multiple immunopathological events occurring at the GI mucosa: early, detrimental, severe CD4(+) depletion in mucosal regions, mucosal immune hyperactivation and inflammation, and intestinal epithelium damage. Previous human studies have shown anti-inflammatory effects of cannabis, along with slowed GI tract disease progression. This project aims to further understand HIV infection and its response to patients’ cannabis use. We hypothesize the anti-inflammatory effects of cannabis should decrease the microbial translocation within HIV+ individuals. Using stool from HIV+ and HIV- patients, DNA and short chain fatty acid (SCFA) extractions were performed. The DNA was extracted using Power Fecal DNA extraction kits. In order to understand microbial community and how it relates to SCFA production, the extracted genomic DNA was PCR-amplified and will be sequenced with an Illumina MISEQ. SCFA extraction was done with ethyl acetate. We analyzed the samples using gas chromatography-mass spectrometry, and it showed HIV+ patients had a decrease in acetic (p=0.0057), propionic (p=0.0325), butyric (p=0.0007), iso-butyric (p=0.0039), and valeric acid (p=0.0133). When compared with HIV- patients, there’s an overall decrease in total SCFA (p=0.0012). These results demonstrate the detrimental effects HIV infection has on SCFA production, which can lead to a decrease in available energy for colon cells and disrupt gut microbial community health. However, amongst HIV+ with cannabis use, we saw an increase in acetic (p=0.0173), propionic (p=0.0087), butyric (p=0.0173), iso-butyric (p=0.0043), and total SCFA (p=0.0057). The HIV+ patients that used cannabis saw improvement in microbial community health, which is a promising sign that cannabis assists with the recovery of antiretroviral treatment.

There is an ongoing movement to improve undergraduate biology courses by elevating student learning beyond rote memorization toward thinking about science as experts do. Previous research indicates that most students leave introductory biology with novice-like perceptions of science. We hypothesize that these scientific ways of thinking can be cultivated in an active learning environment where students take ownership of their learning, and instructors question and facilitate understanding rather than dispense knowledge. In addition, there are no delineations of paradigms of active learning that optimize student learning. In our project, we asked whether student attitudes and expert-like thinking improved throughout an introductory biology course at UW Bothell. In addition, we analyzed the active learning practices in this course to see if these practices correlate with improving student attitudes. During the first and last weeks of class, students voluntarily completed the CLASS (Colorado Learning Attitudes about Science Survey), a 32-piece questionnaire developed by educators at the University of Colorado Boulder inquiring about enjoyment, real-world connections, problem solving and conceptual understanding in biology. We coded results using a published tool, with pre and post data separated for comparison. Classroom lectures were recorded using Panopto, and sessions will be evaluated using PORTAAL (Practical Observation Rubric to Assess Active Learning), a tool that allows for the assessment of the extent of active learning in the curriculum. With this data, we will be able to gauge the effectiveness of active learning methods in an introductory biology class and see if they correlate with a transition towards expert-like perceptions of biology. It is our hope that with this data, these pedagogical techniques can be refined and adopted more widely in academia to help all students succeed in biology.

Diabetes is increasingly prevalent in the world, and there are currently over 29 million people in the United States with diabetes. Type 1 diabetic patients depend on insulin injections to maintain their blood insulin within a certain level so that their cells are getting enough sugar for energy production. Type 2 diabetic patients mostly rely on diet treatments and combinations of insulin and other drug treatments to avoid hyperglycemia. Moreover, type 2 diabetes often leads to different complications such as cardiovascular disease, blindness, and kidney failure. The goal of our study is to investigate insulin effects on the activation of macrophages, which are immune cells with important roles in inflammation. Since a pro-inflammatory state of macrophages can enhance insulin resistance and lead to cardiovascular diseases, it is crucial to understand if insulin changes the macrophage activation states that can cause off target effects leading to other medical complications. The experiments for this project are performed using RAW 264.7 cells, an immortal cell line derived from mouse macrophages. A dose experiment of insulin stimulation was performed to test if phosphorylated STAT1 (pro-inflammatory or M1) and phosphorylated STAT6 (anti-inflammatory or M2) were detected via western blot. Additional experiments determined the intensity of the macrophage response by measuring downstream signaling proteins (PI3K or IRS2) via immunoprecipitation and western blot. Also, RNA extraction and qPCR were performed to see if the gene transcription of macrophage polarization is activated by the above transcription factors. For example,  TNFα and IFNγ were measured for M1 polarization and IL-4 and IL-10 were measured for M2 polarization. Finally, NF-κB, another transcription factor was measured to determine if phosphorylation occurred, which should lead to M1 gene transcription. Together, these experiments revealed whether insulin affects key pro-inflammatory and anti-inflammatory signaling pathways in macrophages.

When discussing the experiences of the Asian American community, certain ethnic subgroups tend to receive more attention, while others are sidelined: people may acknowledge Japanese internment camps or the Chinese Exclusion Act, but not the increasing occurrence of post-9/11 racial profiling targeting South Asians, or the high poverty rate among Southeast Asians. We investigate the consequences of this invisibility threat, the situation in which less prototypical subgroups are ignored and rendered invisible within their superordinate group. Prototypicality is defined as the degree to which a subgroup fits the characteristics that are strongly associated with a superordinate group. A pilot study established that Southeast Asian (e.g., Vietnamese) and South Asian (e.g., Indian) ethnic subgroups are indeed perceived to be less prototypical of the Asian American category than East Asian subgroups (e.g., Chinese). The current study uses a 2 (ethnic identity: prototypical, non-prototypical) x 2 (condition: invisibility threat, control) between-subjects design to investigate the effects of invisibility threat on Asian Americans' racial group identity (i.e., sense of belonging, racial identification) and their relationship with fellow group members (i.e., group solidarity, willingness to form coalitions with other Asian Americans). Prototypical and non-prototypical Asian American students are presented with a Wikipedia article about the demographics of the Asian American community, socioeconomic issues faced by the community, and a few notable Asian Americans. This article is either inclusive of all Asian American ethnic subgroups (control condition), or does not mention students' own ethnic subgroup (invisibility threat condition). We predict that experiencing invisibility threat will decrease non-prototypical Asian American's racial group identity and have a negative effect on their relationship with fellow group members. We hypothesize that prototypical Asian Americans will not be affected. This research has implications for the need to disaggregate Asian American data to reduce invisibility threat among Asian Americans.

Vaccine hesitancy, or negative beliefs and attitudes about vaccines, is a key driver to under-immunization in the United States, which can lead to an increase in vaccine preventable diseases (VPDs). Although adolescents are among the populations at risk for VPDs, little research focuses on vaccine beliefs and vaccine hesitancy in this age group, especially college students. College students have both greater independence and increased autonomy in healthcare decisions including the decision to receive HPV, Tdap, Flu, and meningococcal vaccinations. However, only a small percentage of college students receive all the recommended vaccines. The purpose of this study is to explore and identify factors that influence college student's perceptions about vaccine safety and reliability using cluster mapping. We enrolled 65 current undergraduate college students from the University of Washington, who are between 18 and 23 years old. Participants generated statements about factors that influence college student's perceptions about vaccine safety and reliability. These statements were linked and ranked using Concept System's software (Concept Systems, Inc., Ithaca, NY), and the resulting data was used to generate a cluster map, which was interpreted in focus groups. 25 students participated in generating statements and were 56% female, 44% Caucasian, and have an average age of 19.8 years. After eliminating redundancy, the open ended question yielded 102 unique responses. Examples include: "affordability of vaccinations" and "social media". For the next stage, 25 participants who were 48% female, 52% Caucasian, and have an average age of 19.75 years grouped these statements into clusters. Participants on averaged created 7.5 clusters, which included cluster titles such as: "personal beliefs", "vaccine accessibility", and "media about vaccines". The generated cluster map will provide researchers with invaluable insights that may aid in the development of interventions and may help achieve our long-term goal of increasing vaccine uptake among college students.