Found 6 projects
Poster Presentation 1
11:00 AM to 12:30 PM
- Presenter
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- Anna Li, Senior, Psychology
- Mentors
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- Sapna Cheryan, Psychology
- Ella Lombard, Psychology
- Session
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Poster Session 1
- MGH Commons East
- Easel #28
- 11:00 AM to 12:30 PM
In recent years, organizations have debated whether elements of “white supremacy culture”, including a sense of urgency, may create inequitable environments for people of color. We aimed to empirically investigate whether cultures of urgency in professional settings undermine the recruitment of racially minoritized groups. Undergraduate participants (N = 219) read job advertisements for two jobs: one where urgency culture is highly valued (e.g., “swiftly reset priorities at any given time”) and one with less sense of urgency (e.g., “adjust priorities based on capability”; order counterbalanced). Participants then reported how likely they would be to apply to each job. We hypothesized that individuals from racially minoritized groups will be more likely to apply to lower-urgency jobs over high-urgency jobs. The results show that most participants preferred lower-urgency jobs. However, countering our hypothesis, individuals from racially minoritized groups held more positive attitudes towards high-urgency jobs (e.g., how well they think they'd perform in the job) when compared to white participants. This finding casts doubt on the proposed elements of "white supremacy culture". It urges for more empirical research on how different racially minoritized groups may perceive these elements in work settings. Furthermore, our sample consists mainly of Asian Americans, which does not speak for the experiences of other racially minoritized groups. Our future research will focus on diversifying samples collected.
Poster Presentation 2
12:45 PM to 2:00 PM
- Presenter
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- Ellie Plaster, Senior, Public Health-Global Health
- Mentors
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- Jennifer Davis, Bioengineering, Laboratory Medicine and Pathology
- Isabella Reichardt, Bioengineering
- Farid Moussavi-Harami, Medicine
- Session
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Poster Session 2
- CSE
- Easel #166
- 12:45 PM to 2:00 PM
Dilated cardiomyopathy (DCM) is a leading cause of heart failure around the world. Inherited mutations cause the left ventricle of the heart to enlarge, thinning the heart muscle wall and decreasing the overall function of the heart. In my research project, I will determine if disrupting fibroblast function by knocking out a key developmental signaling factor, p38, can improve, or even reverse, DCM disease characteristics. Specific Aim 1 will be to determine the effects of p38 knockout-induced fibroblast dysfunction on cardiomyocyte function and structural remodeling in late-stage DCM. The rationale is that myocytes in DCM have poor contraction and structurally remodel to longer, thinner morphologies, which occurs in our DCM mouse model around 4 months of age. I expect to see less of these characteristics with the p38 knockout. Specific Aim 2 will assess cardiac fibroblast proliferation and fibrosis in response to disabling cardiac fibroblast function late into the DCM disease process. The rationale is that studying and observing the dynamics of the fibroblast population is critical when understanding the effects of fibroblasts and the p38 knockout model on DCM. In previous studies, the Davis lab identified that cardiac fibroblasts maladaptively respond to inherited DCM mutations in cardiac myocytes, worsening the whole heart. I expect to see less fibroblast proliferation in the p38 model. P38 is essential for fibroblast signaling pathways and functionality, so by knocking it out I will be able to test if fibroblasts are a viable therapeutic target for patients with DCM.
Oral Presentation 2
1:30 PM to 3:00 PM
- Presenter
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- Khushi Yadav, Senior, Neuroscience Mary Gates Scholar
- Mentors
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- Michael Bruchas, Anesthesiology, Pharmacology, Departments of Anesthesiology and Pharmacology
- Nephi Stella, Pharmacology
- Anthony English (aengl97@uw.edu)
- Session
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Session O-2H: Mechanisms Modulating Brain Function
- MGH 231
- 1:30 PM to 3:00 PM
Cannabis use has dramatically increased in response to legalization in the U.S., with U.S. sales jumping 46% from 2019 to 2020. áƒ9-tetrahydrocannabinol (THC) is the primary psychoactive compound in Cannabis, and it has been shown to modify learning and motivation amongst regular users. Learning and motivation are key central processes primarily organized by the prefrontal cortex (PFC) brain region. I sought to test effects of THC on PFC activity during appetitive Pavlovian conditioning in mice- a behavior in which a subject learns to pair two stimuli together over time. Doing so provided much needed insight into learning and motivation under the effect of THC. THC acts on the endocannabinoid CB1 receptor, a presynaptic signaling protein responsible for modulating neural activity throughout the brain, with robust expression in the PFC. To monitor neural activity during behavioral trials, we implanted optic fibers into the PFC and virally expressed biological sensors. We used VGLUT1-Cre mice with a Cre-dependent GCaMP6f sensor to selectively target pyramidal glutamatergic activity during conditioning. We also utilized machine learning tracking software, SLEAP, to analyze behavior through video recordings. In our conditioning paradigm, animals were presented with a houselight and a sucrose reward, which they consolidated an association between after many trials. The mice experienced 5 days of Pavlovian conditioning, and I injected a moderate i.p. dose of THC (5 mg/kg) to one cohort, while another was given a vehicle before undergoing further trials. Our preliminary results showed that glutamatergic activity correlated with learning and association to the cue over time. We expected and observed that THC decreased the signals across the animals and reduced motivation. We categorized THC-induced behavior using SLEAP, a program tracking the mouse’s body parts to capture real-time movement, and found that locomotion decreased and resting behaviors increased in the THC cohort.
Poster Presentation 3
2:15 PM to 3:30 PM
- Presenter
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- Maia Czerwonka, Junior, Pre-Sciences
- Mentors
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- Chantel Prat, Psychology
- Malayka Mottarella, Psychology
- Session
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Poster Session 3
- MGH 241
- Easel #76
- 2:15 PM to 3:30 PM
Individuals differ in how easily they perceive and internally represent visual and verbal information. However, these differences in information processing style are not all or nothing; individuals vary not only in the direction of attentional bias, but also its strength. Prior research found that when forced to choose between competing visual and verbal stimuli, people exhibit different degrees of bias when selecting what information to attend to. The present study examines whether individuals with greater visual or verbal attentional biases, relative to neutral attenders, show different levels of sensitivity to conflict between visual and verbal information during a categorization task. Data will be analyzed from 185 participants who completed a card sorting task in which they were asked to sort stimuli into one of three card suits. Each trial contained visual (shape) and verbal (word) representations of the card suit. On 75% of trials, the word and shape matched (congruent) and the other 25% of trials contained inconsistent information (incongruent). Our analysis will compare response times on incongruent and congruent trials (incongruency effect) in high- and low-biased individuals, to measure conflict experienced. We hypothesize that individuals showing a greater attentional bias towards either task modality will ignore information that is misaligned with their preferred information processing style, resulting in a smaller incongruency effect. These results would suggest that biased attenders have quicker access to the information that aligns with their processing style, while neutral attenders notice both information types and experience conflict when they are incongruent. Alternatively, if attentional bias is unrelated to incongruency effect magnitude, this suggests that people process information similarly, and experience biases only at the decision phase. This study has important implications for understanding how individual differences in information processing style affect how much information individuals process in situations with attentional competition.
Oral Presentation 3
3:30 PM to 5:00 PM
- Presenter
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- Yassin Elkhouly, Senior, Biochemistry Mary Gates Scholar
- Mentors
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- Nephi Stella, Pharmacology
- Anthony English (aengl97@uw.edu)
- Session
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Session O-3F: Informatics and Biology for Human Health
- MGH 254
- 3:30 PM to 5:00 PM
∆9-Tetrahydrocannabinol (THC), the primary psychoactive compound in Cannabis, is responsible for the experience known colloquially as “being high.” Considering its alarmingly high rates of usage, THC’s effects on movement behavior are insufficiently studied. My project addresses this crucial gap in our knowledge by investigating the dose-dependent effects of THC on movement behavior using mouse models in tandem with novel behavioral neuroscience techniques. My research aims to establish a preclinical model for THC-induced impairment, focusing on studying its impact on locomotor control. My main experimental tool is a behavioral linear track, which is a clear glass corridor with a 45 degree-angled mirror placed beneath it. The linear track allows us to create a standardized multi-dimensional environment in which mice are recorded after they are treated with either a control or variable doses of THC. The videos taken of the mice are then analyzed using SLEAP. SLEAP is a machine-learning, pose-estimation algorithm that I helped train to track individual points of interest on the mice, such as the nose, paws, and tail. Behaviors of interest, such as walking, rearing, and grooming, are classified by a random forest algorithm that analyzes SLEAP label data to output identified behaviors. This data is then tabulated and graphed to reflect the dose-dependent changes in behavior elicited by THC. These classifications are also used to further analyze metrics during a represented behavior. For instance, for a walk event, we can utilize positional data from SLEAP to calculate and measure kinematic features such as stride length and limb speed, allowing us to distinguish between an unimpaired and an impaired walk. This computerized analysis approach minimizes human bias, reduces error, and produces exhaustive data that can characterize subtle differences in behavior, like when comparing mice exposed to low THC doses of 0.1mg/kg and 0.3 mg/kg.
Poster Presentation 4
3:45 PM to 5:00 PM
- Presenter
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- Mika Hara, Senior, Biology (Molecular, Cellular & Developmental)
- Mentor
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- Nephi Stella, Pharmacology
- Session
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Poster Session 4
- HUB Lyceum
- Easel #109
- 3:45 PM to 5:00 PM
Various anti-cancer therapeutics, known as microtubule targeting agents (MTAs), target the microtubule, a tube-like structure that is a major component of cell mechanisms including mitosis and maintenance of the cell shape. MTAs selectively bind to tubulin — the building block of microtubule —, disrupting microtubule dynamics and inducing cell death. Despite their known impact on antitumor activity, the precise mechanism by which MTAs promote cell death remains unclear. To understand the efficacy of ST-401 (an MTA drug) as a tumor suppressor, I conduct various assays including drug treatment and Western blot to compare the expression of specific proteins in response to the drug treatments. These assays contribute to understanding cellular processes, molecular interactions, and the effects of various treatments or conditions on cells. Currently, I am being trained to conduct an experiment called XFe Seahorse analyzer. I’m carrying out this experiment to assess how the laboratory-discovered drug affects the mitochondrial function in various cancer cell lines. This experiment aims to determine whether the compound down-regulates mitochondrial function, leading to cell death. I’m leading a project to test a specific fission (cell splitting) protein, DRP1, and how its protein level responds to treatment with ST-401 in two GBM cell lines (resistant and sensitive) and one Colon cancer cell line. DRP1 regulates mitochondrial fission to maintain healthy mitochondrial function. Recently, I found an increase in mitochondrial fission 24 hours after ST-401 treatment in the sensitive GBM cell line, so I’ll further examine DRP1 expression by drug treatment and Western blot to understand these results and see whether ST-401 recruits DRP1, resulting in promotion of mitochondrial division. After DRP1 project, I will expand the project to asses the combination drugtreatment where we combine FDA-approved cancer drug and ST-401 to reflect real-world scenarios, aiming to ensure clinical relevance and safety by studying potential drug interactions.