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Who We Are Is How We Win: Ethnic-Racial Identity as a Universal Developmental Asset for the Culture, the Credits, & College Student Success
Get PDFCompleting college is an educational milestone that has meaningful longer-term implications for students in the U.S. (e.g., economic mobility) and their children (Chetty et al., 2017; Reeves & Krause, 2018). Despite the prevalence of ethnoracially minoritized students in the K-12 and overall U.S. populations, Black and Latine students complete college at lower rates than their peers (Department of Education, 2020; U.S. Census, 2020), thus making economic opportunity harder to attain. College completion and healthy progression into adulthood require similar developmental tasks, e.g., defining one’s career, academic goals, and personal identities (Carnevale et al., 2010, 2013; Chickering & Reisser, 1997; Magolda, 2007). Thus, it is possible that a richer, more complex understanding of personal identity development as it relates to college success, career development, and race/ethnicity (i.e., ethnic-racial identity; Umaña-Taylor et al., 2014) would help close college success gaps. Ethnic-racial identity processes are linked with myriad positive developmental outcomes (e.g., Umaña-Taylor, 2023) and have been leveraged, along with concepts such as campus racial climate (e.g., Hurtado & Carter, 1997; Paris & Alim, 2014), to ground various K-12 reform efforts, collegiate cultural/affinity supports, and culturally relevant/sustaining educator programs. However, less work has explored systematically incorporating ethnic-racial identity, with its multi-dimensional, psychological construction, into models or the practice of college student success. I address this gap in my dissertation by first reviewing leading models for young adult development and college success and presenting a new model of postsecondary success that incorporates ethnic-racial identity. Then, I explored preliminary evidence of the model’s theoretical notions using a nationwide survey of 755 U.S. undergraduate college students—a convenience sample recruited online from multiple U.S. regions. Finally, I assessed the feasibility of bringing an ethnic-racial identity curriculum (i.e., The Identity Project) to college campuses using qualitative interview and survey data gathered during a campus-based pilot study with 48 undergraduate students enrolled at one private college. In doing so, I illuminate possible ways for colleges to leverage student ethnic-racial identity—the fuller, contextualized psychological understanding of race/ethnicity—as an asset on campus and, in turn, increase the probability of all college students attaining educational success and economic opportunity.Educatio
Clarion Fox
No full textClarion Fox is a novel interspersed with real police reports, hospital records, and legal transcripts. It explores the intersection of exploitation and self-destruction in the pursuit of money and atonement.
In mid-recession Queens, a desperate literary agent leaks to the media that his client’s, 21-year-old Clarion “Clara” Fox, sordid debut novel, 191 Night, is inspired by a true story, only to discover that everything, from the libel to the illegal, is true. Scrambling to save his career and maybe her life, he attempts to separate fact from fiction by sorting through her massive paper trail and begins to suspect that maybe this is the ending Clara wanted all along.Extension Studie
Essays in Macroeconomics and Labor Markets
Get PDFLabor markets are a central channel through which households are exposed to macroeconomic shocks. This dissertation comprises three essays that examine and quantify the impact of macroeconomic fluctuations on labor markets in the United States. Chapter 1 studies how individual job destruction decisions spill over to other workers in the labor market. Using variation in the nationwide layoff decisions of large firms across local labor markets, we find that labor market congestion, caused by many firms simultaneously destroying jobs, significantly amplifies the earnings losses of laid-off workers during economic downturns. We further interpret these findings through the lens of a heterogeneous-agent quantitative model with labor market frictions. Chapter 2 investigates how a decline in the compensation investors demand for bearing firm default risk affects the allocation of labor. We show that loose credit market conditions lead more workers to take jobs at financially risky firms. Using variation from both labor market and credit market segmentation, we find that taking jobs at these firms increases workers’ labor income in the short run, but results in large and persistent earnings losses once credit conditions tighten. Chapter 3 studies how the provision of mortgage forbearance helped stabilize labor markets following the 2020 COVID-19 recession. Using variation in financial intermediation frictions across mortgage servicers, we find that mortgage payment deferrals under the federal forbearance program accelerated the recovery of local employment once economic lockdowns were lifted. Our estimates underscore the importance of household liquidity in boosting labor demand during economic downturns.Economic
When Workers Won’t Work: How Scientists, Employers, and Social Reformers Understood and Sought Remedies for Industrial Fatigue and Other Workplace Afflictions, 1910-1940
No full textThis dissertation investigates the history of attempts to ameliorate fatigue and other workplace afflictions in the US in the first half of the twentieth century. Bringing together labor history, business history, and the history of science, this dissertation traces how three communities of researchers attempted to apply the emerging sciences of (I) physiology, (II) time and motion, and (III) mind to measure and resolve the intractable problem of industrial fatigue and related workplace maladies. The third group of researchers, championing a mental approach, succeeded in demonstrating, at least to the business community, that the science of studying workers’ minds, rather than their physiology or time and motion, was the key to resolving the labor problem. I argue how, in this process, these scientific approaches invented to wrangle the condition of fatigue sometimes amplified it, transforming fatigue study from a reform-minded initiative to protect workers’ health to a tool for capital to better command its workforce. By using science to pathologize the mental roots of fatigue, researchers promised industry a method for ensuring peaceful workplaces free from discontent and transformed industrial life. As workers variously resisted, sabotaged, and acquiesced to these new initiatives to scientifically collect data about their behaviors, minds, and bodies, they left behind a history of how workers experienced and responded to technological transformations at work.History of Scienc
From Cell Type to Structure: A Multiscale Framework for Discovering Psychiatric Genes, Pathways and Mechanisms
No full textHuman genetics is perhaps the most fundamental biomarker for neuropsychiatric disorders. While genetic studies have identified numerous risk loci for neuropsychiatric disorders, the biological mechanisms they perturb remain unclear. We generated single-nucleus RNA sequencing (snRNA-seq) data from across multiple human brain regions to weight neuronal co-expression patterns by polygenic heritability, enabling the identification of disease-relevant pathways from common variant architecture. This framework was robustly validated through convergence with rare variant signals from large-scale exome sequencing data across multiple neuropsychiatric disorders, revealing Ca2+ homeostasis as a central and recurrent axis of genetic vulnerability.
Within this pathway, we identified ATP2B2 – a P-type ATPase responsible for Ca2+ extrusion – as consistently downregulated in the prefrontal cortex in donors with schizophrenia compared to controls, both synaptic proteomes and snRNA-seq. This reduction is specific to excitatory neurons, pointing to a cell type-specific loss-of-function mechanism linking ATP2B2 to schizophrenia risk.
ATP2B2 displays a striking enrichment of missense variants implicated in schizophrenia, autism and neurodevelopmental disorders. To investigate the structural basis of this signal, we developed a 3D enrichment framework that leverages the AlphaFold 3-predicted structure to pinpoint structurally constrained mutational hotspots with likely functional impact. We did this by testing for an excess of case-derived variants within 15Å spherical neighborhoods around each residue, and identify compelling candidates for downstream mechanistic interrogation. We identified an enrichment of case-derived
variants localized in close spatial proximity to both the Ca2+ permeation tunnel and binding site and the ATP:Mg2+ coordination site, suggesting two distinct mechanisms of ATP2B2 perturbation. In the Ca2+ binding neighborhood, substitution of the Ca2+-coordinating residue E457 with lysine (E457K) introduces a charge-reversal, suggesting disrupted binding as a focal mechanism of pathogenic variation in ATP2B2. We used AlphaFold 3 to simulate ATP2B2 and Ca2+ with and without E457K, and found it markedly reduced Ca2+ contact probabilities relative to wildtype, supporting an LoF effect.
We validated E457K’s impact in two orthogonal assays. The variant abolished ATPase activity in recombinant ATP2B2 and in a cellular context it impaired Ca2+ extrusion in HEK293 cells using a GCaMP6s-based imaging assay - both consistent with a LoF mechanism aligned with the direction of genetic risk. This suggests that case variants in ATP2B2 very likely compromise its function and disrupt intracellular Ca2+ homeostatic equilibrium. Our study constitutes a significant contribution to the neurobiological elucidation of etiological genetic risk and advances mechanistic insight into the pathogenesis of neuropsychiatric disorders.
First, in a biochemical assay, the variant completely abolished ATPase activity in recombinant ATP2B2. Second, in a cellular model, GCaMP6s-based Ca2+ imaging in HEK293 cells revealed a marked impairment in Ca2+ extrusion, indicative of disrupted Ca2+ clearance. Both findings converge on a loss-of-function mechanism, consistent with the direction of genetic risk observed in neuropsychiatric cases as well as the downregulation seen in functional genomics datasets. These results strongly suggest that pathogenic variants in ATP2B2 compromise its physiological role in maintaining intracellular Ca2+ homeostasis. Our study constitutes a significant contribution to the neurobiological elucidation of etiological genetic risk, and provides a mechanistic link between rare genetic variation and disrupted neuronal Ca2+ signaling, offering novel insight into the molecular pathogenesis of neuropsychiatric disordersBiological and Biomedical Science
Dissecting spatial tumor-immune microenvironment in response and resistance to immune checkpoint blockade in metastatic melanoma
No full textImmune checkpoint blockade (ICB) therapies have markedly improved the prognosis for patients with stage III & IV metastatic melanoma by prolonging progression-free and overall survival rates. However, the variability in mechanisms of immune evasion and resistance present significant challenges in the clinical efficacy of ICBs. This project aims to define drivers of immunotherapy response and resistance by employing advanced genomic, single cell mRNA analyses, and spatial profiling techniques on tissue biopsies from metastatic melanoma patients.
In this study, we developed a framework to analyze response and resistance, both intrinsic and acquired, via immune features in the tumor microenvironment in a standardized, uniformly processed, and deeply clinically annotated cohort of metastatic melanoma patients (n=61) treated with ICB as part of the human tumor atlas network (HTAN) initiative1,2. From the tumor samples, we conducted single-nucleus RNA sequencing, and for a subset of the samples, high-resolution spatial imaging (including protein mIHC, CODEX, and MERFISH transcriptomics). Standardized processing and data pipelines allowed for the integration of genomic, transcriptomic, and spatial features to elucidate characteristics and mechanisms in the tumor microenvironment and their relationships with resistance. For this thesis, I focused on MERFISH spatial transcriptomics analysis.
Single-nucleus RNA sequencing analysis revealed CXCL13+CD4+ T cells and ISG+CD8+ T cells as the strongest predictors of durable clinical benefit (DCB) among all immune populations, independent of clinical confounders. We also identified five recurrent cellular neighborhood modules: extreme responders are enriched in B cell–enriched RCNs with close T–B cell distance, non-responders in tumor–myeloid and tumor–myeloid–stromal interface RCNs, and non-extreme responders in tumor-dominant and stromal–immune interface RCNs. This project integrates transcriptomic and spatial features to elucidate shared tumor and microenvironmental states and their relationships with resistance, guiding more personalized and effective treatment strategies for metastatic melanoma.Graduate Educatio
Leveraging Millimeter-Scale Multi-Material Manufacturing for Biomedical Devices
No full textThis thesis explores the use of precision laminate manufacturing to develop millimeter-scale biomedical devices that enable new capabilities in soft-tissue attachment, biological fluid sampling, and integrated sensing. Millimeter-scale devices are transforming minimally invasive medicine by allowing tools to be ingested, injected, or delivered through natural orifices, accessing previously unreachable areas of the body with minimal trauma. We present three proof-of-concept devices that demonstrate how laminate-based design unlocks new clinical functions. First, we draw inspiration from parasitic organisms such as Taenia sp. to replicate their mechanical anchoring strategies with rotating hook-like elements that latch into tissue with minimal damage. Second, we develop a modular gastrointestinal fluid-sampling capsule designed to collect microbiome-rich samples from hard-to-reach regions of the GI tract. The capsule architecture supports interchangeable modules for actuation, one-way fluid control, sample storage, and triggering. Third, we propose a set of customized sensors tailored to patient-specific anatomy and constraints. These devices are fabricated using multi-material micromanufacturing techniques that combine laser machining, lamination, and origami-inspired folding to integrate complex mechanisms at the millimeter scale. The modular design principles established here provide a foundation for future adaptive, patient-specific, and scalable biomedical tools.Engineering and Applied Sciences - Engineering Science
Morphological analysis of glia-neuron interactions during cochlea wiring
No full textCochlea hair cells, the sensory receptors for hearing, transduce auditory input to electrical signal relayed to the brain via bipolar spiral ganglion neurons (SGNs). SGNs extend a peripheral process (SGNpp) to target one hair cell, and their central processes coalesce with vestibular axons and brainstem efferents to form the eighth cranial nerve. In the mature cochlea, SGN cell bodies are myelinated by satellite glia while SGN peripheral and central axons are myelinated by Schwann cells. SGNpps exit the spiral ganglion at the same time as neural crest-derived glia precursors (GPs) and, after reaching the hair cell region, SGNpps of similar characteristic sound frequency will fasciculate into radial bundles intertwined with GPs. It is not known how radial bundles are formed nor if the tightly associated GPs contribute to SGNpp outgrowth organization during cochlear wiring.
Here we find that GPs extend radially ordered “sawtooth-like” protrusions at the early stage of SGNpp extension. Most SGNpps can be found growing along or behind the glia protrusions, within the same radial domain. This suggests that GPs may play a role in early SGNpp pathfinding. From sparse labeling of GPs early in development, we identified four morphological classes of GPs across the cochlea. These morphologies hint at multiple modes of interaction with SGNpps, other migrating GPs and otic mesenchyme cells that may foster cochlea wiring fidelity. Furthermore, changing interactions between GPs and SGNpps during development may promote radial bundling of SGNpps underlying cochlear tonotopy.Medical Science
Activation-dependent lentiviruses promote selective expansion and transduction of antigen-specific T cells
Get PDFTumor-infiltrating lymphocyte (TIL) therapy has shown recent promise in the treatment of advanced melanoma. However, current manufacturing pipelines make use of bulk-expanded TILs, without the ability to select for bona fide tumor-reactive clonotypes. Thus, new methodologies are required to enhance the selectivity and potency of autologous TILs, while leaving bystander T cells untouched. Here, we demonstrate an approach to target recently-activated T cells via display of agonistic ligands that bind to a marker of early T cell activation (4-1BB, CD137) on the surface of a lentiviral (LV) particle. These pseudotyped LV vectors specifically recognize human 4-1BB in cell lines and primary T cells, promoting the selective activation and expansion of antigen-specific T cells from rare starting populations after antigen stimulation. Moreover, anti-4-1BB LVs specifically transduce antigen-specific T cells with user-defined genetic cargoes that can be used to both track individual clonotypes via single-cell sequencing and enhance their cytotoxic function to extend survival in a xenograft model of human melanoma. We also demonstrate that anti-4-1BB LVs can be directly added to tumor-associated lymphocytes and TIL-containing tumor fragments, promoting the transduction of patient-specific T cells ex vivo. Overall, this platform offers the ability to target antigen-specific T cells (CD4+, CD8+) in an antigen-agnostic, MHC-independent manner with potential applications in adoptive cell therapy manufacturing pipelines and TCR identification efforts.Immunolog
Complete Community Control: A Historical Ethnography of Educational Self-Determination at St. Joseph’s Community School (1969-1985)
Get PDFWhat educational models have African American educators and families developed to combat the pervasive impacts of antiblackness in education? This study explores the practice of self-determined education through a historical ethnography of St. Joseph’s Community School, a women-led, community-controlled institution formerly located in Roxbury, a predominantly Black neighborhood in Boston, Massachusetts. Foregrounding the voices of Black women, I pair the historical methods of archival analysis and oral history collection to explore St. Joseph’s social and historical context, as well as the school’s leadership model, political philosophies, partnerships, pedagogy, and curriculum. As both an institutional history and a social history of Black women and families’ educational activism, the study departs from traditional historical narratives that frame desegregation era Boston as a site of antiblack violence – a discursive practice that overlooks the city as a site of African American agency and organizing. Instead, I draw upon Black feminist theory to argue that Black Bostonian educators, mothers, and perhaps most surprisingly, politically active nuns, engaged in educational leadership as an act of Black Power. In doing so, the school community constructed their own definitions of Black Power that diverged from dominant historical frames of patriarchal and militaristic ideology and centered the development of a rigorous, culturally relevant educational alternative for Black children. This study provides readers the opportunity to rethink the key actors, sites, and practices of the Black Power Movement and to better understand educational practices that foster Black students’ academic achievement and holistic well-being. Ultimately, this study aims to engage the past educational pursuits of Black women and families to inform a justice-based vision for the future of education.Educatio