OSCAR Excellence Award Winners – Page 2 – OSCAR Celebration of Student Scholarship and Impact

College of Engineering and Computing OSCAR

DNA-origami-based biomimetic interfaces for T-cell activation

Author(s): Benjamin Safa

Mentor(s): Remi Veneziano, Bioengineering

Abstract

DNA Origami Nanoparticles, also referred to as DNA-NPs, are nanostructures that take advantage of the Watson-Crick complementary base pairing rules to create precise DNA nanostructures with precise and customizable size and shape within the 10-nanometer to 100-nanometer size range. DNA-NPs provide a highly programmable interface for function as nanocarriers of proteins and are highly biocompatible, allowing them to be administered in vivo as they can be broken down by natural enzymes within the body (such as DNAse). DNA-NPs have also shown significant promise in the realm of T-cell activation, acting as nanocarriers for conjugated tumor antigens and antibodies, allowing for the activation of T-cells and recognition of target antigens (such as those overexpressed in tumor cells). Here, we aim to determine favorable nanoscale organizations of simple DNA-NP motifs—specifically ligand stoichiometry, protein orientation, and position—to determine the efficacy of different T-cell signaling pathways in CD8+ T-cell expansion and proliferation. Building on previous work done under previous URSPs, the previous wheel motif will be utilized in order to move forward with assembling such interfaces. Various protein conjugation methods will be tested with motif—mainly copper free click chemistry techniques, such as DBCO-azide, maleimide-thiol, and NHS/NH2 —and conjugation efficiency will be tested through the use of surface plasmon resonance experiments. Motifs will then be tested with fluorophores/mock proteins (i.e., streptavidin) to verify the nanoscale control of antigen presentation using the DNA Origami technique, most likely through the use of atomic force microscopy (AFM) and fluorescence resonance energy transfer (FRET) experiments. After validating optimal conjugation methods with the motifs, interfaces will be produced with attached cytokines and tested by our collaborator in vitro with CD8+ T-cells.

Audio Transcript

Unknown Speaker 0:01
Ben, hi everyone. My name is Ben Safa, and my project is DNA origami based biomedic interfaces for T cell activation.

Unknown Speaker 0:11
So a key problem in adoptive cell therapy, which is a form of cancer immunotherapy,

Unknown Speaker 0:17
is basically the immunosuppressive environment of the tumor microenvironment and the related cell exhaustion adopted. U cell therapy is a form of cancer where we extract white blood cells from patients, modify them, and then re administer them. And these white blood cells are susceptible to a variety of things, but the main problem that we’re focusing on is cell exhaustion, which causes limited responses across cancers.

Unknown Speaker 0:51
The need for a memory type is integral to solving this problem of cell exhaustion, and

Unknown Speaker 0:59
there have been different types of platforms created for this, but DNA origami is something that may provide a very efficient, scalable platform and very precise platform to solving this problem. DNA origami is basically

Unknown Speaker 1:15
DNA nanostructures that are created through a long, single strand scaffold and several short staple strands that help fold the structure into any arbitrary shape.

Unknown Speaker 1:25
This research thus attempts to create such interfaces,

Unknown Speaker 1:31
namely 2d

Unknown Speaker 1:33
structures to enrich memory like qualities in T cells, in the context of improving adoptive cell therapy and fusion products.

Unknown Speaker 1:43
So the methods we employed for this were one design and two synthesis. We started with a target geometry, in this case a wheel, and used the software predicts to generate scaffold and staple sequences, and we used we ordered those Safa scaffold and scaffold sequences from

Unknown Speaker 2:05
a manufacturer and added different types of

Unknown Speaker 2:10
synthesized the scaffold, first using DNA polymerase and different types of materials such as DNTPs, and added the staple strands to get our final structure.

Unknown Speaker 2:22
Then after that, what we hope to do is attach any type of protein you want. Likely this will be different types of stimulatory ligands, such as 41 BB. This is common

Unknown Speaker 2:35
stimulatory ligand for memory for T cells. We also could attach stuff like fluorophores to track our interfaces and different types of

Unknown Speaker 2:48
beads to characterize these structures,

Unknown Speaker 2:55
so the results that we experienced

Unknown Speaker 2:59
are detailed. So at the top here we have our scaffold synthesis. So we started with a template, primers and additives. So these are DNTPs, which allow us to make the scaffold, and we have a faint Ben at the bottom, which is our single strand DNA, which you want to isolate, as well as our double strand at the top,

Unknown Speaker 3:27
the single strand DNA here is has been purified through centrifugation, and after that, we folded it with our structures, with Our staple strands, and did a variety of different characterization on this at the bottom here, you’ll see a dynamic light scattering graph on the left, then a atomic force microscopy graph image, and then a gel electrophoresis image on the left. Our DLs graph shows the diameter of our particles, and we measured it to be around 58 nanometers, and we got something around that value. So that means it’s consistent. Our AFM images showed that there were some defects in our structure, so that would require us to go back to the staple sequence design, which is what we did and what we’re currently working on. And our gel electrophoresis showed that we were able to successfully purify our structures.

Unknown Speaker 4:27
So

Unknown Speaker 4:29
over the course of the spring, basically what we’ve done is verify the folding of our structures and modify our staple sequences such that we are able to get a structure that does not have the defects that you see in these AFM images. We’ve also proceeded to add overhangs, and we are going to be trying conjugation protocols over this coming summer. Thank you. Applause.

College of Humanities and Social Science OSCAR

Predictors of Young Adults’ Physical Activity and Sedentary Behavior

Author(s): Matthew Burdick

Mentor(s): Jerome Short, Psychology

Abstract

Although cardiorespiratory fitness and muscular strength are the strongest predictors of lifespan examined in epidemiologic and experimental research, over 75% of adults in the United States fail to meet national physical activity (PA) guidelines and many live sedentary lifestyles. Identifying predictors of PA and sedentary behavior (SB) may inform public health interventions. This study uses questionnaire and activity monitor data to identify predictors of PA/SB for young adults. Young adults are an underexamined population within the PA/SB literature and research on this topic has yielded inconsistent findings. Participants (n = 216) were about 20 years old, predominantly female (n = 149), and owned a smart watch. The study transpired over 29 days with a pretest and two posttests. We examined 6 predictors: perceived stress, anxiety, depression, somatic pain, meaning in life, and gratitude. Sitting time was significantly negatively correlated with meaning in life, moderate PA, vigorous PA, and exercise satisfaction. Moderate PA and exercise satisfaction were unique predictors of sitting time. Perceived stress and somatic pain were negatively correlated with vigorous PA and steps per week. Sitting was negatively correlated with days of walking. Exercise satisfaction was a unique predictor of vigorous PA and daily steps. We found bidirectional relationship between perceived stress and vigorous PA that was mediated by exercise satisfaction. Our findings indicate that interventions should focus on lowering sitting time and raising exercise satisfaction to promote young adults’ adherence to CDC PA recommendations. The relationship between psychological factors and PA might be largely explained by exercise satisfaction.

Audio Transcript

Hello everyone. So exercise. We all know fundamentally that exercise is probably good for us. It might make us lose some weight. It might help us be more energetic throughout the day. It even might make us live longer. So why is it so hard for us to exercise? So. Research shows that cardio respiratory fitness, and muscular strength are the strongest predictors of lifespan in the research.

So this beats cancer risk. This beats smoking risk. This beats type two diabetes. If you can run fast and hard and you can lift heavy, you will likely live for a long time. Despite this, over 75% of adults in the United States fail to meet the national guidelines. So why is this the case? So our question was, what are the mental and physical factors that predict exercise and sitting behavior, especially in young adults?

And the way we attacked this question was we recruited over 200 Mason students who with a mean age of 20 years old, and we required them to wear smartwatch smart watches throughout a 29 day period. And now throughout that period we analyze their sort of different psychological and physical variables through questionnaire data.

And after that study we were able to run data analysis using SPSS.

So what predictors or did we examine in this study? So we examined sort of two classes of predictors that we hypothesized to be either protective or harmful to physical activity. So protective. We have meaning in life. So the sense that someone feels that they can engage purposefully in their day-to-day lives, sort of the antithesis to nihilism.

And now you have gratitude is gratitude can be a state and a trait so people can feel grateful. All of the time. Or they can have moments where they feel gr grateful, which is more of the trait like gratitude. Um, this questionnaire measures both the state and the trait, but it basically means how grateful are you or like how much gratitude do you have for your current situation despite all the negatives.

So it’s sort of like almost an optimistic worldview. We also have several risk factors, so perceived stress. Anxiety, somatic symptoms and depression. Somatic symptoms meaning bodily pain and aches.

So what do we hypothesize?

First things first, we hypothesize that the risk factors, so remember, that’s your perceived stress, anxiety, depression, and body pain. We predicted that that would be. Um, related to less exercise and more sitting. So for example, someone who is very anxious, we expect them to exercise less and sit more. And this is in line with the research.

Um, uh, alternatively, we think that the protective factors, so those are our median life and gratitude will be related to more exercise and less sitting. Finally, we predict that all these factors to both risk and protective factors will uniquely predict exercise in sitting. So that means that out of all the variables that we assessed in our study, we would think that the, all our protective and risk factors accountant for unique variants in our outcomes.

So what we observe. Our relationship between our predictors and outcomes is primarily attributed to our factors instead of some other confounding third variable. So what do we find? So first we found some pretty interesting information about our samples activity. So again, we have about 200 Mason students over 18 years old.

With a mean age of 20 years old, and we found that GMU students surpass Americans in meeting C to C guidelines. So that means that you can see in our figure here that almost 54% of American, or sorry, 54% of GMU students meet or exceed the national guidelines of activity. So the CD. C recommends that people, especially adults, more specifically.

Participate in at least 150 minutes. So two and a half hours of moderate intensity exercise per week, or the equivalent of vigorous activity. And so we found that in our sample over almost 54% of our students met or exceeded these guidelines. Whereas nationally, only 25% of American adults meet those guidelines.

So we’re almost twice as compliant. Compared to the average American, but this can be somewhat misleading because as you can see on our bottom bar here, the sedentary bar, almost 20% of GE students in our sample had zero minutes, zero minutes of activity per week. And so that was a cause for concern.

We found that meaning in life was negatively related to sitting time. So people who perceive that they have a purposeful engagement in their life, that they can traverse the day-to-day events of their life and feel like it has purpose. Those people tended to sit less throughout this 29 day period.

We also found that people who were physically active, especially within the moderate physical activity category, um, this uniquely predicted sitting time up to 29 days after baseline. So basically this was our big longitudinal finding that people who were. Especially active at day one of our study tended to sit less up to almost a month after baseline.

Additionally, we found that perceived stress and somatic pain were negatively related to vigorous activity and daily steps. So people who reported being more stressed and having more bodily pain, typically exercised less and walked less.

So exploratory analysis revealed some interesting results. So especially before examining the relationship between stress and vigorous activity. As you can recall, before we found that stress was negatively related to physical activity, but uh, exploratory analysis revealed that stress was not a unique predictor of vigorous activity, meaning that.

There’s something else accounting for that variance. And what we found was exercise satisfaction accounted for that variance in a bi-directional, fully mediated model. So what does that mean? It means that perceived stress has no relationship, uh, has at least no unique relationship with vigorous activity.

But when you include exercise satisfaction. It has a mediaing relationship so that, so in our first model here in Model A, we found that people who were stressed reported less exercise satisfaction and exercise satisfaction. Being a strong predictor of vigorous activity would increase vigorous activity.

So basically, people who were stressed had less as facts from exercising, and so were less likely to exercise. Additionally, this was bidirectional. So if you flip it on its head, it is also true. So vigorous activity has no unique predictive relationship with perceived stress, but when you add exercise satisfaction, vigorous activity can, is, can be associated with a lot of exercise satisfaction.

And in doing so since exercise satisfaction is, is, um, associated with less perceived stress. It can vigor activity, could then could lead to less perceived stress. I should state that this is cross-sectional data, so we’re not making a causal claim, but we did find a fully mediated cross-sectional model with these variables, some things to take away with you.

So median life is negatively related to setting time. So. If you can find a way to increase your perception of life being purposeful to you, that things aren’t meaningless, that your actions matter. If you can increase that, you may be able to sit less and improve your physical health. Um, being active, especially moderately active, decreases your risk of sitting for chronically amount, chronic amounts of time.

Uh, stress may reduce exercise satisfaction, which in turn would reduce your, um, vigorous physical activity and vigorous activity may raise exercise satisfaction. And finally, satisfaction is weigh in more vigorous activity. Thank you for listening. Have a good day.

College of Science OSCAR

A Non-Invasive Buffer Based Alternative to DNA Extraction from Teeth

Author(s): Fatima Durrani

Mentor(s): Joseph DiZinno, Forensics

Abstract

In forensic and anthropological contexts, DNA extraction from teeth is critical in cases where individuals must be identified from mass disaster sites, crime scenes, or ancient skeletal remains. Traditionally, the standard method adopted by the FBI and forensic laboratories is an invasive one, involving the drilling, crushing, or creating a powder of the tooth to access DNA within the dentin. This approach is impractical, since the tooth is a piece of evidence and can be important for analysis in the future. My study aims to provide a non-destructive alternative. I followed a protocol proposed by Monalisa Heng and Éadaoin Harney, using a guanidine-based buffer to extract DNA without damaging the tooth. Cleaned third molars were placed in the buffer, leeching DNA out of the cementum. This buffer proved successful, extracting DNA suitable for analysis, demonstrating that non-invasive extraction is a feasible alternative to destructive techniques. Additional research should be done in the future, including DNA sequencing to assess the quality and completeness of the genetic material. In addition, sodium or potassium acetate buffers could also be tested for comparative studies of non-invasive DNA extraction

Audio Transcript

Hello everyone, my name is Fatima Durani. I am a biology major and a forensic science minor. Or rather I have a minor in forensic science I conducted my research under the guidance of Dr. Madden in the biology department. I am a predental student as you can probably tell from my research so let’s get straight into it. My research focus is on a non-invasive buffer-based method of DNA extraction from teeth you’re probably asking Fatima why the heck are you doing research on teeth so some up when it comes to ancient remains or mass disasters where corpses are decay beyond identification, forensic scientist Take the teeth of these corpses extract DNA from these teeth and identify individuals, however All these scenarios have one thing in common can be used as evidence fortunately, the standard protocol to extracting DNA from these teeth is to destroy the truth. Now this visual I included actually is a minimally invasive method where the tooth is drilled and the DNA is extracted that way once it’s placed in the buffer however, in many cases, the entire tooth is destroyed and into a powder. And DNA extracted that way this is impractical when you’re looking as teeth as a source of evidence for future analysis So a solution to this issue is a buffer-based extraction protocol, which is what my research focuses on I used a buffer proposed by Mona, Lisa, Hank and Dr. Harney So this buffer includes guineas HCL which help DNA extract from the tooth while preserving the pH in the integrity of the DNA so as you can see here, I included a visual that shows you that the pulp in the Denton this pink flesh inside the tooth contain most of the DNA in the in invasive protocol which includes crushing the tooth aims to extract DNA from this area however, DNA is also included in the cement in the enamel, which is the outer portion of the tooth The invasive method that I will use that the invasive method that I will use using the buffer plants to extract DNA from this cement in the enamel, especially around the root right here, so the invasive protocol includes powder rising. The tooth placing get a protein is buffer and then quantify it using PCR. The noninvasive method includes emerging in a buffer created right here and then purifying the DNA quantify it using PCR and then and then both results or both DNA extractions from both methods will be analyze and analyze using gel electrophoresis This is just me. I gonna be so loud because teeth can contain diseases so I worked under a hood. This is the invasive method that I used crushing the juice to extract the DNA. This is the buffer and the that was placed in the buffer and this was me just cleaning the truth with. To remove any debris or blood so ask for the results in the conclusions the gel for the noninvasive method actually showed a successful amount of DNA these bands represent DNA at the 450 base pair Portion Well, one well one was the negative control which was just a buffer and two was the positive control which was a swab of my cheek and then the remaining well not including the ladder were the third molars that were placed in the buffer and DNA was extracted that way Invasive method actually was supposed to be a control method that had a positive result however, as you can see deep, something went wrong. There is no bands like the invasive method and there are two but they’re very faint so the likely reasoning behind this was. When I placed the powder in the button the Chex buffer I placed too much tooth powder, which let you contamination. Some future improvements to the study. Include adding DNA sequencing to check for contamination. Using degraded samples to allow my buffer to be implemented in anthropological settings and testing other buffers such as sodium and potassium acetate, which are stronger and more likely to extract more DNA from the acknowledgments. I’d like to know who is my mentor Doctor Who ordered all of materials necessary for this project and Dr. Madden for providing the lab and the resources I needed to conduct my research. As for the work protocol, buffer were inspired by Mona Lisa Hayes study on the development of non-invasive DNA extraction method. Definitely check her study and research out. It’s very interesting. She worked on dog teeth thank you guys so much for listening to my little research. Blurb have a nice day.

College of Humanities and Social Science College of Science OSCAR

Pharmacological Characterization of Chimeric NMDA Receptors in Xenopus

Author(s): Diborah Gutema

Mentor(s): Theodore Dumas, Department of Psychology, Interdisciplinary Program in Neuroscience

Abstract

NMDA receptors (NMDARs) play a critical role in synaptic plasticity and cognitive function by mediating both ionotropic and non-ionotropic signaling. During postnatal development, NMDA receptors undergo a subunit shift from GluN2B to GluN2A, a transition associated with synaptic maturation and the emergence of mature cognitive function. While previous research has explored the physiological and behavioral consequences of this transition, the specific mechanisms driving these changes remain unclear. In particular, the relative contributions of ionotropic and non-ionotropic signaling have not been fully defined. Ionotropic signaling involves calcium influx through the receptor channel upon ligand binding, while non-ionotropic signaling refers to intracellular signaling cascades initiated by conformational changes in the receptor that occur independently of ion flow. This study aims to dissect these signaling pathways by utilizing chimeric GluN2 subunits engineered to separate ionotropic and non-ionotropic functions. Chimeric constructs are currently being subcloned into Xenopus laevis–compatible vectors for functional expression in oocytes. This work has involved preparation of the pGEMHE-membrane-EGFP backbone through bacterial culture and plasmid isolation via alkaline lysis mini prep, followed by gel electrophoresis and spectrophotometric analysis to assess plasmid integrity and purity. Restriction digests were performed to linearize the plasmid and confirm backbone identity. In parallel, GluN2A, GluN2B, and chimeric constructs have been cultured from glycerol stocks and are currently undergoing PCR amplification with construct-specific primers. Following amplification, the inserts will be digested, purified, and ligated into the vector. Preliminary results confirm successful plasmid preparation, and insert amplification and ligation are ongoing. Once subcloning is complete, the constructs will be injected into Xenopus laevis oocytes, followed by two-electrode voltage clamp (TEVC) recordings to measure receptor responses to varying concentrations of glutamate and glycine, as well as pharmacological modulators of NMDA receptors. Statistical analyses using two-way ANOVA will compare current amplitudes across receptor type (GluN2A, GluN2B, ABc, BAc) and treatment condition (agonist/modulator concentration), with the goal of identifying distinct electrophysiological profiles associated with each subunit composition. This study will characterize how differences in GluN2 subunit composition and intracellular domain identity affect NMDA receptor-mediated signaling in an isolated system.

Audio Transcript

Hello all. I am Diborah Gutema and this is my video presentation for my project, Pharmacological Characterization of Chimeric NMDA Receptors in Xenopus laevis Oocytes.

NMDA receptors are ion channels located on neurons that allow calcium ions to enter the cell when activated by the neurotransmitter glutamate. This calcium signaling, known as ionotropic signaling, is critical for synaptic plasticity, learning, and memory. NMDA receptors can also engage in non-ionotropic signaling, where conformational changes in the receptor trigger internal signaling pathways without ion movement. Each receptor is composed of two GluN1 subunits and two GluN2 subunits. A developmental shift occurs where GluN2B subunits are gradually replaced by GluN2A, a transition essential for synapse maturation. Understanding how these subunits contribute to ion flow and conformational signaling is the focus of our project.

To investigate how different regions of NMDA receptor subunits contribute to signaling, we are working with chimeric GluN2 constructs developed by Dr. Dumas’s lab. These chimeras are engineered by swapping specific intracellular domains between the GluN2A and GluN2B subunits. In doing so, we can separate the functional contributions of individual regions, such as the intracellular tail, to ion flow and to non-ionotropic signaling. By studying receptors with these controlled domain swaps, we aim to determine which portions of the subunit structure are responsible for differences in calcium permeability, activation properties, and downstream signaling. This semester, we focused on preparing the DNA constructs necessary for expressing these receptors in Xenopus laevis oocytes for future functional testing.

The overall goal of this project is to express wild-type and chimeric NMDA receptors in Xenopus laevis oocytes and compare their ionotropic signaling properties using two-electrode voltage clamp recordings. By analyzing how domain swaps between GluN2A and GluN2B affect receptor function, we aim to better understand the molecular basis of NMDA receptor signaling. This semester, we focused on preparing high-quality plasmid DNA, optimizing restriction digests, and initiating PCR amplification of the GluN2 receptor inserts to prepare for future subcloning and expression studies.

First, upon receiving the plasmid pGEMHE-membrane-mEGFP, we transferred a sample from the backstab into a 3 mL bacterial culture, which was incubated overnight at 37 degrees Celsius for 16 to 24 hours. The plasmid includes a Xenopus laevis promoter sequence, which enables later expression in oocytes. Following incubation, we isolated and purified the plasmid DNA from the bacterial culture using a alkaline lysis mini prep protocol. To ensure the integrity and purity of the plasmid, we assessed DNA quality using agarose gel electrophoresis to check for intact plasmid structure and spectrophotometry to measure the 260/280 absorbance ratio.

Next, we performed restriction digests to prepare the plasmid for future subcloning. We used the enzyme NheI to linearize the plasmid and carried out diagnostic digests to prepare for the later excision of the GFP segment originally present in the vector.

In parallel, we grew bacterial cultures containing the DNA for GluN2A, GluN2B, ABc, and BAc constructs. Using these templates, we initiated PCR amplification with construct-specific primers to selectively amplify the inserts. PCR amplification is currently ongoing. Once complete, we will purify the amplified products and verify insert size by gel electrophoresis before moving on to the next phase of subcloning.

After the inserts are fully amplified and purified, we will digest them with restriction enzymes to create compatible ends with the plasmid vector. We will then use a DNA ligase enzyme to join the inserts and vector together, creating new plasmids that carry either the wild-type or chimeric NMDA receptor sequences. Some ligation reactions will be performed in-house, while others may be sent for commercial cloning depending on efficiency. Sequence verification will follow to confirm successful ligation.

Following sequence confirmation, we will synthesize capped RNA transcripts from the recombinant plasmids using in vitro transcription. These RNA molecules will then be injected into individual Xenopus laevis oocytes, allowing the cells to produce functional NMDA receptors for electrophysiological testing.

Two to three days after RNA injection, we will perform two-electrode voltage clamp recordings, a technique that holds the membrane potential constant while measuring ionic currents. By applying glutamate and glycine, we will evaluate receptor function based on current amplitudes, activation and deactivation kinetics, and dose-response characteristics. Comparing wild-type and chimeric receptors will help us determine how specific subunit regions influence NMDA receptor ionotropic signaling.

This semester, we focused on growing bacterial cultures, isolating and purifying plasmid DNA, troubleshooting purification and digestion protocols, and beginning PCR amplification of the NMDA receptor inserts. These steps are critical for setting up RNA synthesis, oocyte injection, and functional testing. Moving forward, we aim to complete subcloning, synthesize RNA, and characterize receptor function using TEVC recordings.

I’d like to take a moment to thank those who have been instrumental in this project.

Dr. Herin who has been an invaluable mentor in electrophysiology and molecular biology.

Dr. Dumas who has provided expert guidance on receptor signaling and chimeric constructs.

Hannah Zikria-Hagemeier who was essential in training me on plasmid preparation.

Finally, I’d like to thank the rest of the PBNJ Lab for their collective support through guidance and resources, which has been key to my growth as a researcher.

Thank you all for your help and support!

College of Engineering and Computing OSCAR

Developing an Affordable Open-Source Bionic Hand

Author(s): Robert Haas

Mentor(s): Nathaila Peixoto, Electrical and Computer Engineering

Abstract

This project explores the feasibility of developing an affordable, open-source, bionic prosthetic hand to develop an alternative to be used in applications where traditional prosthetics are not an option. Developing a functional prototype based on proportions taken from a human hand provided a solid foundation for the rest of the project. The initial prototype served as a testbed, allowing me to test different methods of control. Such as input from an electromyography amplifier and accelerometer module, that when processed by an Arduino microcontroller can be used to control servos that open and close the hand. The project aims to provide a functional prototype, design schematics, and CAD models as reference material. To be used by others in the pursuit of developing and delivering non-traditional prosthetics options.

Audio Transcript

INTRO:
Welcome to a brief overview of my Undergraduate Student Research Project, Developing an Affordable Open-source Prosthetic Hand.

BACKGROUND:
The initial prototype I designed was part of a group project for my introduction to engineering class. It was controlled by a mobile app that connected to a microcontroller via Bluetooth module. This prototype had several shortcomings, most notably the single motor set up didn’t deliver enough power to close the hand properly. This issue was compounded by the hand’s lack of flexibility.

SECOND PROTOTYPE:
When developing the second prototype, I mitigated these problems with additional motors on the back of the hand and included a horizontal joint in the upper half of the palm, allowing the hand to flex.

FINGER DEVELOPMENT: 20 sec (show pictures of finger prototypes and them video of them flexing)
When designing the fingers, I developed multiple prototypes to test different tolerances for the hinge joints. I used dual pivoting joints for the fingers to increase flexibility and extended the supports on the back of each of the links to prevent them from flexing backwards.

MATERIALS
I tested multiple materials for this project including PLA+, PETG, and Resin. Resin provided the highest level of detail with resin. However, the most practical option was PETG. It’s stronger and more heat resistant then PLA+, and unlike resin it can be printed on a standard FDM printer.

CONTROL METHODS
I experimented with multiple control methods, using an off the shelf electromyography amplifier, also known as EMG, and custom-built amplifier. I was able to control the hand using the input from an accelerometer module. When the module detects a tilt the motors wind mono filament line closing the hand. When the module is tilted back the motors spin the opposite direction, unwinding the line and opening the hand. One area for improvement is with the EMG amplifier. I was unable to control the hand using input from the EMG amplifier.

CONCLUSION
There are some improvements that can be made to the project. Specifically, further testing of the EMG component as well as exploring other methods of control, to provide diverse control options to potential users. Additionally, certain components of the hand such as the cable guides and elastic retainers could be redesigned to print as one piece. This would also reduce and optimize the materials needed to construct it. I would also like to integrate a Bluetooth component to the hand, to allow the user to configure specific gesture presets through an app.

College of Humanities and Social Science College of Science OSCAR

Secretory Mitophagy Exports p53: A new pro-tumor survival mechanism.

Author(s): Layla Hasanzadah

Mentor(s): Purva Gade, Center for Applied Proteomics & Molecular Medicine

Abstract

Mitochondrial dysfunction is associated with many life-threatening illnesses, from Parkinson’s disease to malignant cancers. Cells remove damaged, aged, or stressed mitochondria through a process called mitophagy. Our team is investigating a potential pro-tumor survival mechanism cancer cells enact with the help of mitophagy initiation and subsequent export. Mitophagy initiation is sensed by the molecule PINK1, triggering the isolation and packaging of the damaged mitochondrial segment for degradation through the lysosome. Cancer cell mitophagy is triggered by elevated oxidative stress and mitochondrial DNA damage caused by hypoxia, chemotherapy, radiotherapy, and immunotherapy. In our recent study, we discovered a secretory form of mitophagy in which damaged mitochondrial segments are packaged and exported outside of the cell within PINK1+ extracellular vesicles (EV). Additionally, we found that these PINK1+ EVs export tumor suppressors (TS) phospho-P53 and Merlin along with mitochondrial segments outside the tumor cell. It has been discovered that p53 is phosphorylated by PINK1, ultimately enhancing mitophagy. We also found that Merlin, an unappreciated TS associated with neurofibromatosis, interacts with p53 through the MDM2 mediator. We hypothesize that secretory mitophagy export of TS and other mitophagy-related proteins is an adaptive mechanism of cancer cells to withstand oxidative stress and avoid apoptosis. The export of TS p53 and Merlin were analyzed in 4T1 & IOMM-Lee cells. We isolated EVs via differential ultracentrifugation followed by immunoprecipitation of purified EV samples with PINK1 and phospho-p53 to identify protein-protein interactions. Western blotting and mass spectrometry were performed to validate immunoprecipitation results and PINK1 and p53 interaction. Understanding the role of EV-mediated export of TS in secretory mitophagy can reveal novel mechanisms aiding cancer cells’ survival under oxidative stress caused by chemotherapy or other treatments, offering potential therapeutic targets for various cancers.

Audio Transcript

Mitochondrial dysfunction is associated with many life-threatening illnesses, from Parkinson’s disease to malignant cancers. Cells remove damaged, aged, or stressed mitochondria through a process called mitophagy. Mitochondria are known as the powerhouse of the cell for a reason: they help produce the majority of the energy needed to power our cells. In Parkinson’s disease, scientists have found that the process of mitophagy is impaired, leading to an accumulation of dysfunctional mitochondria within cells. On the other hand, in cancer cells, mitophagy plays a more complex role and may even be enhanced. As evidenced by my research, our lab at the Center for Applied Proteomics and Molecular Medicine found that the process may serve as a kind of survival mechanism used by cancer cells in the face of oxidative stress caused by chemotherapy or radiation.
Mitophagy initiation is sensed by the molecule PINK-1, triggering the isolation and packaging of the damaged mitochondrial segment for degradation through the lysosome. Our team discovered a secretory form of mitophagy in which mitochondrial segments are packaged and exported outside of the cell within extracellular vesicles (EVs) derived from the interstitial fluid of breast cancer tumors. Moreover, it has been discovered that the tumor suppressor molecule p53 interacts and becomes phosphorylated by PINK-1, ultimately enhancing mitophagy and carcinogenesis. Pancreatic cancer (PC) p53 mutations are associated with tumor aggressiveness. Decreased levels of intercellular p53 leads to increased genetic instability, higher tumor growth rate, and survival. Pancreatic cancer is the 3rd most fatal cancer in the U.S. due to high rates of metastasis and late diagnoses. Understanding and targeting this imbalance may result in new forms of personalized medicine for PC patients.
In terms of materials and methods, I cultured PANC-1 and BXPC-3 cell lines and incubated them for 5 days, then applied a drug called CCCP to each flask. CCCP induces oxidative stress to mimic the conditions experienced by cancer cells undergoing treatment like chemotherapy or radiation. Afterwards, I confirmed that I had protein in my sample, and used various stages of ultracentrifugation to isolate the extracellular vesicles produced by these cells. The vesicles came in 3 sizes: 2K (the largest), 10K, and 100K (the smallest). To analyze the proteins within my samples, I used Western Blotting and mass spectrometry, and used the ExoView R200 to examine and categorize the EVs used in the experiment.

Here you can see some images of me working in the lab: doing cell culture, running Western Blots, and observing my pancreatic cancer cells.

My project produced some very interesting results. I compared the relative concentrations of p53, the tumor suppressor protein, and PINK-1, the mitophagy-associated signalling molecule, and found that there is a very high and positive correlation between the export of PINK-1 p-p53 via EVs when oxidative stress is induced, indicating that p53 is degraded and exported alongside PINK-1 in EVs.Exported p53 may aid tumor progression and constitute a novel diagnostic method of non-invasively determining the mitochondrial health and p53 status within PC. PC EVs positive for phospho-p53 represent a novel diagnostic biomarker indicative of tumor stress. Targeting EV pathways in combination with oxidative stress could be a novel method of treating PC. Our lab is currently investigating if secretory mitophagy & EV export of tumor suppressors is common among other kinds of cancer, as well.

We recently published a paper on the topic of secretory mitophagy, but again, we hope to connect secretory mitophagy to the export of other tumor suppressors in future studies.

I wanted to thank my mentors and colleagues at the Center for Applied Proteomics and Molecular Medicine for their continued guidance and support, including the following people: Purva Gade, my direct mentor, Dr. Lance Liotta, Dr. Marissa Howard, Sofie Strompf, Angela Rojas, and Thomas Philipson.

I would also like to thank the GMU OSCAR URSP program and Dr. Karen Lee, as I received funding and guidance from OSCAR throughout the past semester.

Thank you very much for listening to my presentation!

College of Visual and Performing Arts OSCAR

Pompeii

College of Engineering and Computing OSCAR

Hagley Library & Archive Management

Author(s): Soo Yoo, Nguyen Pham, Ayan Diraye, Matthew Walsh, Maha Kaleem, Matteen Mahfooz

Mentor(s): Gail Therrien, IST Department

Abstract

Our capstone project involved working with the Hagley Museum & Library in Delaware, U.S. We enhanced the processes for Hagley’s archive inventory management to enable smoother operations for pulling and returning research materials, as well as viewing statistical information. We carried out this project because we value Hagley’s pursuit in supporting innovative research and hope to positively affect the processes for both archivists and researchers.

Audio Transcript

College of Engineering and Computing College of Science OSCAR

THE DIRTY CONSEQUENCES OF POOR SLEEP: MODELING GLYMPHATIC EFFICIENCY ACROSS DIVERSE SLEEP-WAKE CYCLES QUALITY.

Author(s): Alvaro Olmo Jimenez

Mentor(s): John Robert Cressman, Department of Physics and Astronomy, Krasnow Institute for Advanced Studies

Abstract

The glymphatic system plays a vital role in maintaining brain health by facilitating the clearance of metabolic waste, a process most active during sleep. This clearance is facilitated by changes in extracellular space due to glial and neuronal shrinkage, enabling enhanced flow of interstitial and cerebrospinal fluid. The relation between the change in brain volume and the effectiveness of the glymphatic system has already been described. Despite the evidence linking sleep to brain clearance, the relationship between the quality of the sleep-wake cycle and glymphatic system efficiency remains unexplored. Thus impeding the understanding of how disrupted sleep may increase vulnerability to neurodegenerative diseases by impairing brain waste clearance. This study investigates the relationship between sleep-wake cycle quality and glymphatic system effectiveness by utilizing an existing computational model of neural dynamics. We calibrated the model to replicate real brain activity – matching frequencies and activity with data collected through EEG– during healthy NREM and REM sleep. These cycles were modeled and their response in brain volume change examined to assess the performance of the glymphatic system. Then, parameters – such as ionic conductance or vascular volume– were modified to simulate poor or high-quality sleep-wake cycles and the glymphatic system’s response examined. Early findings suggest that high-quality sleep cycles induce higher volume changes and therefore better glymphatic performance. Nevertheless, further analysis is required to more fully assess the system’s behavior across all sleep conditions.

Audio Transcript

Hello everyone. My name is Álvaro Olmo Jiménez, and today I’ll be presenting my research on THE DIRTY CONSEQUENCES OF POOR SLEEP: MODELING GLYMPHATIC EFFICIENCY ACROSS DIVERSE SLEEP-WAKE CYCLES QUALITY.
First, we will start by explaining why we are doing this research. Basically,we know that there are established links between sleep and brain clearance. The glymphatic system acts as the brain’s cleaning system and during sleep changes in glial and neuronal cell volume expand the extracellular space, which promotes convective fluid flow and waste clearance. Nevertheless, the specific impact of sleep quality on the glymphatic functions remains unexplored. This knowledge gap limits our understanding on how disrupted sleep may contribute to neurodegenerative disease risk
Thus, this study aims to explain how the quality of the sleep-wake cycles affect the glymphatic system during sleep.
To do so, we first established what was going to be our indicator for sleep quality → Brain volume change. This is because variations in extracellular and intracellular volumes during sleep enhance the glymphatic performance. Also, because the release of sleep-promoting molecules like prostaglandin induces blood vessel dilation and further volume changes.
At this point, we could state that our main focus was to study how the volume change is affected by varying the sleep-quality.
Once we had our indicator for good sleep, we used an existing model of neural dynamics implemented with glial dynamics whose behavior is determined by the concentration of ions.
This model was calibrated to replicate real brain activity – matching frequencies and activity with data collected through EEG. For example, a frequency of 2.8Hz was used to simulate NREM and 5.6Hz to simulate REM.
Moreover, we used an electrical and a volume stimulation as parameters to determine the sleep quality. The higher these parameters, the higher the simulated sleep quality. Therefore, from a bigger volume stimulation, a bigger volume change and thus the better glymphatic performance.
In order to replicate regular sleep, we did numerous simulations. However, just the most significant ones are going to be shown.
In this figure we can see 3 different simulations. In the three of them, the same electrical stimulation is used. The difference between the high and low volume stimulation is that the stimulation effort is halved. We can observe that over 20 cycles, there is not a significant brain volume change if we don’t stimulate the volume and that there is some difference in the final volume depending on the stimulation.
Now, we can see the transmembrane potential change for the high volume stimulation. One can see that the voltage deeply decreases with the volume stimulation. This makes sense because while the volumes vary, ion concentration varies too. Thus, we can state that the alterations of pump dynamics and diffusion result in a decrease in the transmembrane voltage.
In this figure, which again outputs high volume stimulation over the last cycle of the simulation, we can clearly appreciate the change in frequency from NREM to REM with the change in volume. Also, for further visualization, the right has been done and the change in frequency revealed.
From these figures, which show the change of concentration of intracellular sodium and extracellular potassium over the last cycle between electrical and non-electrical simulation outputs, we can see how electrical stimulation is fundamental for the correct simulation of sleep dynamics. Although it does not seem that important for volume change, we can see that in the simulation with electrical stimulation there is a balance between the intracellular and extracellular potassium and sodium. While in the non electrical-stimulated run, there is no apparent difference. This happens because the ATP-pump is shut-off due to the low extracellular potassium and thus cannot transport these two ions correctly. Although these ionic effects may not seem that important, they can be highly significant, as they can alter the signalling properties of the neuron.

This figure shows how the overall volume change varies if the sleep quality is disrupted. It is important to remark that in the microarousals simulation, 3 random intervals ranging from 1 and 5 seconds for each cycle were done and volume stimulation was stopped. Something similar was done for the less quality sleep simulation. In it 3 random intervals ranging from 5 and 15 seconds for each cycle were done and volume stimulation force was halved.

We can see the final values for each volume in this next figure.

Although it seems that the volume decrease is higher in the simulation with microarousals – suggesting that it has better glymphatic performance than varying sleep quality simulation – it is not. This is because the microarousals last less than the low stimulation stages. Thus, the simulation (with microarousals) would have less volume decrease if both periods– microarousals and low stimulation stages– lasted the same.

Now, from this data we can conclude that as sleep quality decreases, we observe a reduction in both overall volume changes and thus in glymphatic efficiency. This is consistent with previous findings that link slow-wave activity and stable sleep patterns with enhanced interstitial fluid movement and metabolic waste clearance.

Moreover, while volume stimulation contributes to mechanical shifts in brain tissue, electrical stimulation proves essential for preserving ionic balance. Without it, ATP-dependent pumps like the sodium-potassium pump become ineffective, leading to disrupted ion gradients and impaired homeostasis.

This underscores the critical role of electrical activity in maintaining proper cellular function, beyond just facilitating volume changes. The breakdown of ionic regulation in the absence of electrical stimulation highlights the interdependence of mechanical and electrophysiological processes in sleep. Together, these findings reinforce the complexity of accurately simulating sleep.

Ultimately, further research is needed in order to flawlessly replicate sleep, accounting not only for volumetric shifts and electrical rhythms, but also for how these elements dynamically interact over time. Accounting for the metabolic rate of the pumps.

College of Humanities and Social Science OSCAR

The Effects of Young Blood Plasma on NfL and GFAP following Traumatic Brain Injury Administration in Wild-type Mice

Author(s): Timothy Kochany

Mentor(s): Jane Flinn, Psychology

Abstract

Traumatic brain injuries (TBIs) are a major health concern, with there being over 200,000 TBI related hospitalizations in 2020. Repetitive mild TBIs (rmTBIs) lead to cumulative effects, worsening damage. Previous research demonstrated that young blood plasma transfusions may reverse factors of neurodegeneration in older populations, those with Alzheimer’s Disease, and those with TBIs.
Glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are proteins that act as biochemical markers that can be detected in blood to observe astrocyte activation and axonal integrity. Previous studies have shown that TBIs can induce neuronal death and contribute to neurodegenerative disease.
GFAP is a protein expressed by astrocytes that is involved in the injury repair of brain tissue. Overexpression of GFAP has been shown to correlate with lesion volume and TBI severity, as well as astrogliosis in releasing inflammatory mediators, such as cytokines and reactive oxygen species (ROS). This is part of the process of secondary injury during rmTBI. Neuroinflammation is a factor that contributes to neurodegeneration. This is pertinent because GFAP has been known to reflect glial responses to neuroinflammation.
Similarly, NfL is a protein found in the axon of neurons and is released into the plasma when injury or neurodegeneration is present. NfL is involved with structural support and aids in the conduction speed of action potentials. In previous studies, elevated levels of GFAP and NfL have been shown to signal the progression of neurodegeneration.

Audio Transcript

Hi everyone. My name is Tim Kochany. I’m a third-year neuroscience student at George Mason University and my project is The Effects of Young Blood Plasma on Neurofilament Light Chain and Glial Fibrillary Acidic Protein following Traumatic Brain Injury Administration in Wild-type mice. In the year 2020 alone, there have been reported over 200,000 hospitalizations related to traumatic brain injuries. This is a major world health concern because traumatic brain injuries have been known to lead to neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, as well as cognitive decline. Previous research has demonstrated that plasma from young mice injected into older mice has seemed to rescue deficits induced by traumatic brain injuries. My research focuses on two proteins that are involved in this process: Glial Fibrillary Acidic Protein, or GFAP, and Neurofilament Light Chain, or NfL. Glial Fibrillary Acidic Protein is a protein that is expressed by astrocytes and is involved in the injury repair process of the brain. Similarly, Neurofilament Light Chain is a protein found in axons, which is a part of the neuron that helps propagate the signal from one neuron to the next, and overexpression of this protein has been shown to signal the progression of neurodegeneration. Repetitive mild traumatic brain injuries lead to cumulative effects, worsening brain damage. Prior to the current study, plasma injections and saline injections have been administered and the mice have been euthanized and plasma samples have been collected. There are four groups of mice: TBI plasma, TBI saline, sham plasma, and sham saline. Sham is if no TBI has been administered. For the procedure, I am going to be looking at and I’m going to be using Enzyme-linked Immunosorbent Assay or ELISA to detect protein quantities in the plasma from these mice. For this process, antibodies for the specific protein are going to bind to that protein and then we are going to detect protein concentrations by shining a specific wavelength of light through the sample. My hypothesis is that traumatic brain injuries will increase levels of both GFAP and NfL, with the groups receiving plasma injections slightly lowering these concentrations. This research has significant implications for the study of neurodegeneration and public health relating to traumatic brain injury treatment. Unfortunately, no results are available at this time, as I’ve had errors with our ELISA microplate reader malfunctioning to collect data. However, data will be available at the OSCAR poster celebration on May 6. If you would like to see a full list of my works cited, you can scan this QR code here.

College of Humanities and Social Science OSCAR

Is Executive Function Similarly Related to Behavioral Outcomes in Typically Developing and Neurodiverse Children? A Meta-Analysis.

Author(s): Armita Dadvar

Mentor(s): Sabine Doebel, Psychology

Abstract

Executive functions (EFs) are a set of neurocognitive processes that support goal-directed thought and action. EFs are essential to child development, especially in its concurrent and longitudinal relation to both academic achievement (Allan et al., 2014; Blair et al., 2015; Spiegel et al., 2021) and school readiness (Blair & Razza, 2007). Research suggests that children diagnosed with neurodevelopmental conditions show greater impairment in EF compared to their neurotypical peers (All, et al., 2024). The project investigated the relation between EF in young children and behavioral outcomes by conducting a mixed-effects meta-analysis. It explored whether the relation between child EF and behavioral outcomes varies depending on whether children are typically developing or have clinical, learning, or behavioral diagnoses. Detailed inclusion criteria were established and we conducted a systematic literature search across four academic databases. Abstract screening was performed to identify papers that meet the inclusion and exclusion criteria for the study. All eligible studies were identified, and the data was coded and analyzed with the help of MetaReviewer. For statistical analysis, we used CHE modeling through the metafor and clubSandwich packages on R-Studio. Results indicated no significant association between executive function and internalizing or externalizing symptoms, but a small significant trend linking better EF to fewer hyperactivity and inattention behaviors. No significant differences were found between neurodiverse and neurotypical children. However, better EF was significantly related to fewer externalizing problems in children with ADHD, and younger age was associated with a stronger EF–behavior relationship. These findings suggest that EF may be a modest intervention target for early behavioral difficulties, with future research needed to explore diagnostic-specific patterns and increase study representation for neurodivergent populations.

Audio Transcript

Hello everyone, my name is Armita Dadvar and this presentation is on my Honors Psychology Thesis titled “Is Executive Function Similarly Related to Behavioral Outcomes in Typically Developing and Neurodiverse Children?” which I completed with my advisor Dr. Sabine Doebel. Have you ever heard of the term executive function? Executive functions are the set of neurocognitive processes that help us engage control over our thoughts and actions, manage and retain the information in our brains, preventing undesirable thoughts and behaviors while prioritizing ideas and actions that are aligned with personal objectives. You might be thinking, why is executive function important to study in childhood? It is important because research has shown that executive function rapidly develops through childhood and essential to child development. It even has concurrent and longitudinal relation to academic achievement and school readiness. It also may be a key path through which socioeconomic status influences academic outcomes. Lastly, It is even believed to be more malleable than IQ and other general cognitive capacities and thus a good target for interventions. Over many years, numerous tests have been conducted by researchers to carefully evaluate EFs as they arise through childhood. Although we understand that EF is is related to many behavioral outcomes in typical developing children, we do not know if these relations are similar for children who are neurodiverse or have learning, behavioral, or clinical diagnoses that implicate brain areas supporting EF. The current project investigated, via a meta-analysis, the relation between EF in young children and behavioral outcomes, and whether the relation between child EF and outcomes varies depending on if children are typically developing or neurodiverse. Our research question is: Does the relation between child EF and behavioral outcomes vary depending on the population under consideration? We hypothesized that there will be stronger, more consistent executive function/outcome relations in neurodiverse vs neurotypical samples. For this meta-analysis, we were specifically interested in early childhood, executive function and related moderators, key moderators of population, socioeconomic status, age and gender and lastly three main behavior outcomes or externalizing, internalizing, and inattention/hyperactivity. in terms of methods, we first finalized the inclusion and exclusion criteria, then we conducted searches across 4 different bases. After collecting results from those searches, we screened a smaller percentage of abstracts and determined which do or do not meet the inclusion criteria. All eligible abstracts moved on to full text coding through Metareviewer. For statistical analysis, we used CHE modeling to account for dependency among effect sizes. We ran the models with the rma.mv() function from the metafor package in R and calculated robust test statistics using the coef_test() function from the clubSandwich package. This approach gives more accurate variance estimates and properly handles the fact that some studies contributed multiple effect sizes. We found no significant relationship between executive function and internalizing and externalizing symptoms. However, there was a small-to-moderate significant trend suggesting better EF might be linked to fewer hyperactivity and inattention symptoms.In terms of our hypothesis, we did not find meaningful group differences between neurodiverse and neurotypical children in these relationships.When exploring moderators, we found better EF was significantly related to fewer externalizing symptoms in children with ADHD. However, no strong associations were found for hyperactivity/inattention in ADHD or for group differences between ADHD and typical samples. We also found that the EF-behavior relationship became weaker as children got older. No effects were found for the sex moderator and SES could not be analyzed due to too much missing data. Our results suggest that better executive function may be modestly linked to fewer hyperactivity and inattention symptoms in young children, consistent with previous research. Future research should expand the number of studies, especially for neurodivergent children, examine specific diagnoses separately, and evaluate potential publication bias to strengthen conclusions. Thank you so much to my advisor, Dr. Sabine Doebel, the Developing Minds Lab, and my committee members Dr. Jennifer Brielmaier and Dr. James Maddux for their expertise and guidance throughout this project. Thank you to OSCAR for the funding of this project through the URSP. Lastly, here are my references and thank you all for listening.

Carter School for Peace and Conflict Resolution OSCAR

Feasibility of Implementing “Sponge City” Concepts in Gangnam, Seoul, to Mitigate Flood Risk

Author(s): Dayeon Shin

Mentor(s): Dakota McCarty, Department of Environmental Science & Policy

Abstract

Urban pluvial flooding, intensified by the climate crisis, poses escalating challenges for cities worldwide. In 2022, Gangnam District in Seoul, South Korea—a high-density, economically critical area—suffered catastrophic flooding, particularly between Gangnam Station and Seocho 2-dong. Contributing factors included low-lying topography, outdated drainage systems, and insufficient green infrastructure. To address these vulnerabilities, reliance on traditional grey infrastructure must shift toward integrated nature-based solutions, such as those advocated by the Sponge City model pioneered in China. This study analyzes the Gangnam and Seocho-Gu districts to identify the most influential variables driving flood risk and to strengthen predictive modeling for future events. A public survey of Seoul residents further informs local perceptions and priorities for urban flood mitigation.

Audio Transcript

This is the final presentation for the URSP program, which is the feasibility of implementing a sponge city concept in Gangnam, Seoul to mitigate flood risk. I’m Dayeon Shin, majoring in global affairs and this research is supported by professor Dakota McCarty from the department of environmental science and policy. Before I go through my research results, I want to give the background of this research briefly. In 2022, Gangnam district, which is a highly and economically developed area, experienced massive urban floods. The primary reasons pointed out lack of green spaces, outdated drainage infrastructure, and low-lying geographical features. To resolve this problem, the Sponge City concept can apply to mitigate urban flooding by expanding the green spaces. The sponge city is based on the nature based system to mitigate runoff water in highly developed cities and it is initiated from China.
I used the quantitative research method, which is public survey and data analysis, SHAP value identifying the most influential variables causing urban floods and collecting Seoul residents’ opinions.
So, in the results for the SHAP value, how the geographical elements affect the urban floods, so we can predict the urban flood based on the high influential elements rank. First is building_count, which is the most influential element with the high number of buildings affected by urban floods in the research areas. The second is the distance of road and river, which indicates that the more far from the road and river, it has less vulnerability in urban flood due to the aging or insufficient drainage systems, which means traditional draining focused on the fast draining. The downstream and NDBI which indicates the grey infrastructure were the following influential elements.
Next is the result for public acceptance from the survey. Over 50% of people do not believe Seoul’s current flood management strategies are effective, and do not trust local government authorities to effectively manage flood risks and people think that the Gangnam district office’s role is the most crucial. Additionally, through the survey, insufficient drainage systems, lack of green spaces, and inefficient urban planning were selected as top 3 challenges in the current flood management policy. Furthermore, the poor coordination among government agencies would be the main barrier.
In conclusion, making balance between green and grey infrastructure is a crucial solution and based on the former environmental policy development of Seoul, enforcement will be needed in making certain spaces for green in the building and parklet or using Chicago green alley as a green infrastructure can be applied as solutions to prevent it. No enforcement in constructing green spaces, no gangnam residents future safety.
These are my references, it was an honor to have this opportunity and thanks to huge support by Prof. McCarty, I hope this research contributes to the future flood prevention in Gangnam, Seoul.