{"id":5040,"date":"2026-03-09T11:59:13","date_gmt":"2026-03-09T15:59:13","guid":{"rendered":"https:\/\/krieger.jhu.edu\/ursca\/?p=5040"},"modified":"2026-03-10T09:08:23","modified_gmt":"2026-03-10T13:08:23","slug":"deans-aspire-grantees-announced","status":"publish","type":"post","link":"https:\/\/krieger.jhu.edu\/ursca\/2026\/03\/09\/deans-aspire-grantees-announced\/","title":{"rendered":"Dean’s ASPIRE Grantees Announced"},"content":{"rendered":"\n

The Office of Undergraduate Research, Scholarly, and Creative Activity is pleased to announce the recipients of the 2026 Dean’s ASPIRE Grants<\/a> (Arts and Sciences Projects, Investigations, and Research Endeavors). These awards are designed to promote independent research projects among our exceptional undergraduate students in the Krieger School of Arts and Sciences (KSAS). Each recipient receives up to $5,000 for a one-year grant period (May 2026 to May 2027) in which they will pursue original research, work closely with a Hopkins faculty mentor, and advance knowledge for the world.<\/p>\n\n\n\n

The 2026-2027 Dean’s ASPIRE Grantees are:<\/h2>\n\n\n\n

Sam Bae ’27 <\/strong>(Molecular & Cellular Biology; Public Health Studies)<\/h3>
\n

“Optimizing TrkA Agonist Dosing to Promote Tendon Regeneration While Preventing Heterotopic Ossification”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Aaron James (SOM)<\/p>\n\n\n\n

Tendon injuries have limited intrinsic healing capacity and often result in fibrotic scar formation and chronic functional impairment despite surgical repair. Recent studies have identified the nerve growth factor (NGF)\u2013TrkA signaling pathway as an important regulator of musculoskeletal regeneration, and pharmacologic activation of TrkA using the small-molecule agonist gambogic amide (GA) has been shown to enhance tendon healing in vivo. However, the dose-dependent effects of TrkA activation remain poorly defined, and excessive pathway activation has been implicated in pathological outcomes such as heterotopic ossification, limiting translational application. This project investigates how TrkA signaling intensity governs the balance between regenerative tendon repair and aberrant tissue formation. Using a murine flexor tendon injury model, the effects of graded GA dosing on tendon healing and underlying molecular signaling will be evaluated. GA will be administered at biologically relevant doses selected based on prior in vivo studies and preliminary data demonstrating divergent healing outcomes. Tendon repair will be assessed through histological organization, biomechanical strength, and expression of tendon- and cartilage-associated markers. To establish mechanistic causality, TrkA pathway engagement will be quantified by analyzing phosphorylated TrkA and downstream ERK and AKT signaling, with pharmacologic TrkA inhibition used to confirm pathway specificity. Local and systemic delivery strategies will also be compared to distinguish tendon-specific effects from indirect influences of innervation and vascularization. By defining a dose-dependent therapeutic window and its molecular basis, this project aims to provide a mechanistic framework for safe TrkA-targeted therapies in tendon repair, with broader implications for pathway-guided regenerative medicine.<\/p>\n<\/div><\/div>\n\n\n\n

Joshua Choi ’27<\/strong> (Public Health Studies; Molecular & Cellular Biology)<\/h3>
\n

“Decoding Autonomic Influence on Hematogenous Metastasis in MC38 Mouse Model: Immunological Characteristics and Metastatic Potential”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Malcolm Brock (SOM)<\/p>\n\n\n\n

Colorectal cancer is the third leading cause of cancer mortality in the United States, with hematogenous metastasis (dissemination through the bloodstream) being the most common mechanism tumor cells spread through to induce lethal pulmonary metastases (in the lung). This project investigates how autonomic nervous system activity \u2014 specifically elevated sympathetic nervous system signaling (your body\u2019s involuntary \u201cfight or flight\u201d response) \u2014 influences hematogenous metastasis utilizing an immunogenic MC38 colorectal cancer model that causes an immune response in mice. Despite growing interest in how neuroimmune crosstalk (how the nervous and immune system influence each other), there is a crucial gap in the lack of in vivo models that directly relate sympathetic overactivity and its influence on quantifiable metastatic outcomes. By establishing a high metastatic hematogenous MC38 tumor line, I aim to test whether sympathetic activity alters the early seeding niche (the early time periods when circulating tumor cells arrest in the lung subject to clearance by cytotoxic surveillance) as well as later metastatic markers by comparing wild type mice to transgenic mice that represent sympathetic overactivity. Specifically, I will conduct flow cytometry to profile the immune system\u2019s changes that support metastasis\/cancer progression and RT qPCR as well as immunohistochemistry to measure invasion\/quantify metastatic burden. By establishing causality and mapping immune\/molecular mediators, this essential work will yield actionable targets and inform neuro-immunotherapeutic strategies (such as adrenergic signaling blocking) to mitigate metastatic progression.<\/p>\n<\/div><\/div>\n\n\n\n

Alexandria Flynn ’27 <\/strong>(Biophysics; Earth & Planetary Sciences)<\/h3>
\n

“Characterizing Baltimore\u2019s \u2018Pistachio Tide\u2019 using Genomics and Geochemistry”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Maya Gomes (KSAS)<\/p>\n\n\n\n

Baltimore\u2019s \u2018Pistachio Tide\u2019 is a recurring phenomenon in the fall where large swaths of the Inner Harbor\u2019s water appear to turn a pale, green color and emit a rotten egg odor. While the green color is often assumed to be the result of an algal bloom, heightened levels of chlorophyll that would indicate such a bloom are not detected. We hypothesize that changes in water color and odor are reflective of green sulfur bacteria(GSB), microorganisms that are green in color and thrive in the presence of sulfide, which emits rotten egg odor. GSB use bacteriochlorophyll, which are not detected by chlorophyll sensors, to perform anoxygenic photosynthesis. The source of sulfide sustaining the microbial bloom is undetermined and could be sulfide accumulated in bottom waters during the summer, or sulfate-reducing microbes continuously supplying sulfide to the sunlit zone. This project will characterize the microbial composition of the Pistachio Tide through 16S rRNA and metagenomic sequencing before, during, and after a Pistachio Tide event in October 2025 from sampling areas throughout Baltimore\u2019s Inner Harbor. National Aquarium water quality data, USGS hydrological data, and Baltimore Social-Environmental Collaborative weather data will be used to contextualize microbial dynamics. Sulfide concentrations, sulfate concentrations, and sulfur isotope compositions will be analyzed, which can provide insights into source(s) of sulfide during Pistachio Tide events. This project investigates how microbial community dynamics and geochemical cycling lead to Pistachio Tide events, which will help to predict future Pistachio Tide events and other bacterial blooms in other densely populated coastal areas.<\/p>\n<\/div><\/div>\n\n\n\n

Anastasiia Malykhina ’28<\/strong> (Neuroscience)<\/h3>
\n

Faculty Mentor: Kimberly Smith (SOM)<\/p>\n\n\n\n

Anorexia nervosa (AN) is life\u2011threatening, and relapse after inpatient refeeding remains common. Inpatient programs provide repeated, structured opportunities to practice eating avoided foods, yet clinicians lack an objective way to quantify the food\u2011specific \u201cdose\u201d of consummatory exposure patients accumulate, and whether that dose predicts reductions in anxiety\u2011to\u2011eat and longer\u2011term outcomes. I developed a pipeline that converts routine unit meal documentation (menus and meal tickets) into standardized exposure variables (one exposure = one standardized portion of a specific food consumed) and links these exposures to clinical outcomes. Aim 1 will refine, audit, and transfer this extraction and standardization pipeline to an independent treatment center to test portability across documentation formats and replicate dose-response associations with anxiety\u2011to\u2011eat and symptom change. Aim 2 will use the Johns Hopkins cohort with assessments at admission, discharge, and 6\u2011month follow\u2011up to identify baseline predictors of short\u2011 and long\u2011term responsiveness using elastic net regression with nested cross\u2011validation. Deliverables will include an auditable, shareable exposure\u2011tracking tool and a predictor set to support more individualized, evidence\u2011based refeeding and exposure planning.<\/p>\n<\/div><\/div>\n\n\n\n

Nishad Okutoyi ’28 (Neuroscience)<\/h3>
\n

“Morphometric and Lineage Characterization of Rod- and Spindle-Shaped Cells in the Developing Human Dentate Gyrus<\/strong>“<\/p>\n\n\n\n

Faculty Mentor: David Nauen (SOM)<\/p>\n\n\n\n

During infancy and early childhood, the dentate gyrus of the hippocampus, a brain region essential for learning and memory, undergoes extensive structural and cellular remodeling. Within this window, a transient population of rod- or spindle-like cells is continuously observed in post-mortem tissue. Despite being observed for decades, their identity and significance remain unresolved. An early study characterizes these cells as microglia associated with perinatal hypoxia. A more recent study found no microglial marker expression and proposed a neural progenitor identity. Neither study investigated the cells\u2019 morphology in detail nor tested for additional lineages. This research will determine the identity of these cells and what governs their transient presence in the developing human dentate gyrus by combining quantitative morphometric analysis\u2014systematic measurement of cell shape, orientation, and position\u2014with immunohistochemistry and complementary molecular approaches across human hippocampal samples spanning mid-gestation through three years of age and hence generating the first detailed profile for this population. By doing so, I aim to resolve longstanding ambiguity regarding the identity of these cells and to define their developmental trajectory in space and time.<\/p>\n<\/div><\/div>\n\n\n\n

Alex Pan ’28 (Molecular & Cellular Biology)<\/h3>
\n

“Investigating the Role of DNA Polymerase \u03b1 in Epigenetic Regulation of Human Induced Pluripotent Stem Cells”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Xin Chen (KSAS)<\/p>\n\n\n\n

DNA replication is an essential and defining aspect of life, allowing for the accurate transmission of genetic information through generations. During replication, DNA is synthesized by polymerases on both the leading and lagging strands, creating an identical copy of the genome before cell division. It has long been thought that replication should not be tampered with, as altering this process often results in adverse effects like cancer and aging. Unexpectedly, our lab has found that reducing the activity of a major lagging strand polymerase, DNA polymerase alpha (Pol\u03b1), leads to beneficial phenotypes like increased fertility in Drosophila and C. elegans, increased resistance to chemical exposure and radiation in Drosophila, mice, and human cells, and increased reprogramming efficiency of differentiated human cell types to induced pluripotent stem cells (iPSCs). However, the mechanisms of this improved cellular health and resilience is still unknown. Therefore, my goal is to determine the cellular and molecular mechanisms of the improved cellular health and resilience resulting from the reduction of Pol\u03b1. I will use human cells and Drosophila as complementary model systems to study Pol\u03b1, with Drosophila serving as a tool to study whole-organism effects (lifespan, fertility, starvation resistance), and gene expression changes (using RNA seq), and human cell culture as a translational model to study cellular reprogramming and re-differentiation for patient-specific cell therapies. This project will increase our understanding of the fundamental process of DNA replication and while translating this knowledge to develop regenerative therapies.<\/p>\n<\/div><\/div>\n\n\n\n

Akhila Rao ’28 (Public Health Studies)<\/h3>
\n

“Manufacturing Demography: Investigating the Role of Racist and Sexist Attitudes in Support for U.S. Pronatalist Policies”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Kris-Stella Trump (KSAS)<\/p>\n\n\n\n

U.S birth rates have declined over the past two decades, contributing to growing concern on its repercussions among the general public and shifting attention towards the pronatalist movement. The pronatalist movement encourages childbirth and reproduction while elevating the persona of motherhood for purposes of demographic manipulation. While existing scholarly literature on pronatalism highlights the racist and sexist motivations embedded in institutionalized pronatalism, little research examines whether these same factors shape the general public\u2019s attitudes towards pronatalist policies in the United States. This study aims to fill such a void in research on pronatalism by investigating whether racial resentment and ambivalent sexism predict individual support for Pronatalist policies, specifically when the latter are framed using racist and sexist narratives. This study will be conducted through an online public opinion survey measuring racial resentment, attitudes towards women, partisanship, and an experimental vignette design that manipulates the narratives used to frame a proposed pronatalist policy. Responses will be empirically analyzed via OLS regression. Ultimately, this research will inform outreach, monitoring, and advocacy narratives for organizations championing gender equity and reproductive rights while simultaneously establishing factual evidence regarding the existence of a relationship between racism, sexism, and support of pronatalist policies. Future research will be able to build on the findings from this project to better safeguard women\u2019s equality and bodily autonomy.<\/p>\n<\/div><\/div>\n\n\n\n

Satviki Shankaran ’27 (Neuroscience)<\/h3>
\n

“Oligodendrocyte lineage-specific restoration of Arid1b expression rescues myelination defects in the Arid1b haploinsufficiency mouse model of ASD”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Brady Maher (SOM)<\/p>\n\n\n\n

ARID1B encodes for the SWI\/SNF chromatin remodeling complex, which is critical during neural development, and is considered a high confidence ASD risk gene. Haploinsufficiency of ARID1B and other SWI\/SNF complex members is strongly associated with Coffin Siris Syndrome (CSS), a neurodevelopmental disorder, characterised by intellectual disability and developmental delay. Despite ARID1B being a high confidence ASD risk gene, the cell type-specific and developmental consequences of ARID1B haploinsufficiency remain poorly understood. Preliminary studies in CSS mouse models (Arid1b+\/-; Pdgfra-cre::Arid1b+\/flox) have revealed disruptions in the oligodendrocyte (OL) lineage, including altered proportions of oligodendrocyte precursor cells (OPCs) and mature OLs and reduced density of myelinated axons in the corpus callosum. In this proposal, we will test the hypothesis that OL lineage-specific reinstatement of Arid1b will rescue the OL lineage, myelination, and behavioral deficits in a CSS mouse model. First, we will validate our newly generated Cre-gated Arid1b reinstatement mouse model (Arid1b-LoxP-GFP-Stop-LoxP; Arid1b+\/LSL) by demonstrating its ARID1b haploinsufficiency, recapitulation of previously observed OL lineage deficits, and Cre dependent restoration of Arid1b expression. Reduced ARID1B expression will be assessed using western blots, qPCRs, and immunostaining at multiple developmental timepoints. Altered OPC\/OL density will be quantified using immunostaining of postnatal day 28 cortex and CC. To test causality, rescue experiments will then be performed by generating Pdgfra-cre::Arid1b+\/LSL to excise the STOP cassette, and restore wild type Arid1b expression in the OL lineage. Rescue efficiency will be evaluated by assessing OPC\/OL density, CC myelination, and behavioral outcomes.<\/p>\n<\/div><\/div>\n\n\n\n

Lana Swindle ’27 (Writing Seminars; Philosophy)<\/h3>
\n

“On the Outskirts of Agency: Assessing the Universality of Gewirthian Natural Rights”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Lucy Allais (KSAS)<\/p>\n\n\n\n

In Reason and Morality, Alan Gewirth developed a secular theory of natural rights. His theory posited that humans, by virtue of being rational agents, are naturally endowed with rights to the necessary conditions that enable them to be successful agents\u2014namely, freedom and well-being. In his work of political philosophy, however, he argued that the freedom of individuals with limited agency should be restricted. This suggests that Gewirth\u2019s natural rights are not universal\u2014rather, they depend on capacities or qualities that are unevenly distributed among persons. While scholars have criticized Gewirth\u2019s theory on logical or naturalistic grounds, few have challenged its lack of universality. I seek to take on this task with the following question: Is Gewirth\u2019s theory compatible with restrictions on freedom for individuals with limited agency? If so, what form of universality does his theory secure and if not, what revision best preserves a secular foundation for universal rights? I aim to answer this by 1) analyzing Gewirth\u2019s central texts (Reason and Morality and The Community of Rights) to fully understand his account of natural rights and the groups he excludes from them; 2) reviewing secondary sources that critique and defend his theory in order to determine whether his limited scope is justifiable; 3) perusing the literature on the rights of agency-limited individuals, and 4) analyzing how alternative natural rights theories approach the problem of universality. Through this reading, I seek to test whether the scope of Gewirth\u2019s theory is justified to develop a solid theoretical foundation for natural rights.<\/p>\n<\/div><\/div>\n\n\n\n

Katrina Wang ’27<\/strong> (Molecular & Cellular Biology)<\/h3>
\n

“Unraveling the TATA-box binding protein: The role of its N-terminal region in piRNA biogenesis”<\/strong><\/p>\n\n\n\n

Faculty Mentor: John Kim (KSAS)<\/p>\n\n\n\n

Although only 3% of the human genome is involved in protein synthesis, recent research revealed that 75% of genes are expressed by transcription into non-protein-coding RNA. A class of these molecules is PIWI-interacting RNAs (piRNAs) that regulate gene expression in reproductive cells. Defective piRNAs can disrupt development of reproductive organs and fertility. Despite the conserved functions of piRNAs, the mechanisms that produce them diverge across species. In round worms, piRNA transcription involves the binding of the small nuclear RNA activating protein complex (SNPC) to piRNA genes. Our lab identified the TATA-box binding protein, TBP-1, as a potential SNPC interactor. TBP-1 is a common general transcription factor, but its role in regulating piRNA expression is unknown. Unlike basal transcription that utilizes the C-terminal core of TBP-1 for DNA binding, piRNA transcription likely utilizes other regions of TBP-1 to associate with the SNPC. Specifically, the disordered N-terminal region of TBP-1 may be involved in specific protein-protein interactions required for the assembly of transcription initiation complexes. Therefore, I will investigate the hypothesis that the N-terminal region of TBP-1 interacts with the SNPC to promote piRNA transcription. In this proposal, I will (1) design a TBP-1 N-terminal truncation series by CRISPR, (2) verify the mutants by immunoblotting and fertility assays, and (3) characterize the truncated N-terminal TBP-1 and SNPC interaction by co-immunofluorescence staining and co-immunoprecipitation. Studying the TBP-1 and SNPC relationship gains insight into a novel mechanism for regulating piRNA expression, and investigating piRNA biogenesis may reveal potential targets for therapeutics in treating infertility.<\/p>\n<\/div><\/div>\n\n\n\n

Yingjun Zhao ’28<\/strong> (Molecular & Cellular Biology)<\/h3>
\n

“Diagnosis as a Gateway to Care? Medicalised Framings of Alzheimer\u2019s Caregiver Burden”<\/strong><\/p>\n\n\n\n

Faculty Mentor: Alexandre White (SOM)<\/p>\n\n\n\n

Family caregivers provide the majority of care for individuals with Alzheimer\u2019s disease (AD), yet their distress is often addressed through medical frameworks that stress individual treatment over structural support. This project investigates how caregiver distress is interpreted within clinical encounters and how medicalized framings affect access to different forms of support. Using a comparative mixed-methods design, the project combines policy analysis, ethnographic observation, caregiver burden measures, and semi-structured interviews with approximately 50 unpaid AD caregivers in the Baltimore metropolitan area. Interviews explore caregiving demands, experiences of distress, the trajectories caregivers follow when seeking care, and the perceived alignment between caregivers\u2019 needs and the support offered. Findings will identify how subjective burden measures and clinical screening practices influence referral pathways and whether they reflect caregivers\u2019 own assessments of need. By showing differences between caregiving demands and available support, this study aims to inform assessment and referral practices that prioritise caregiving intensity and unmet need over psychiatric diagnosis, with implications for clinical care, Medicare, and Medicaid policy in our aging population.<\/p>\n<\/div><\/div>\n","protected":false},"excerpt":{"rendered":"

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