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MEMS 4110: Electric Vehicle Charger Extender
No full textThe goal of this project was to design an extendable mast for a receptacle/connector EV charging unit to help people with disabilities charge their cars more conveniently by automating the process
MEMS 4110: ASME Waste Collection Challenge
No full textMake a remote-controlled vehicle that can traverse the course below (obeying traffic laws), collect garbage units from collection bins and deliver the garbage units to a receptacle
Tests Without Borders: A Global Approach to Measuring Visualization Literacy
No full textVisualization literacy assessments shape how we understand people\u27s ability to interpret data, yet most existing instruments embed Western datasets and assumptions that limit their relevance for global audiences. This thesis argues that because data is personal, assessments must also be culturally grounded. We introduce a unified framework for adapting the Mini-VLAT into 22 regionally responsive short-form assessments, each retaining the structure of the original test while incorporating datasets and scenarios tailored to specific regions around the world. To demonstrate how such adaptations can be customized and validated, we present a detailed case study of a Ghana-adapted Mini-VLAT, developed in collaboration with local teachers and designers. The Ghana version preserves the cognitive skills of the original instrument while embedding locally meaningful data. Psychometric analysis shows that it is reliable (omega = 0.73) and correlates moderately with the original Mini-VLAT, providing initial evidence that culturally grounded instruments can maintain comparability. Altogether, this thesis offers both a global repository of adapted items and a validated country-specific example, providing a cohesive foundation for building inclusive, culturally relevant visualization literacy assessments
Integrating Molecular Electrochemical Insights and Device Engineering: Innovations in Organic Redox Flow Batteries, Methanol-Hydrogen Peroxide Fuel Cells, and Electrochemical Hydrogen Pumps
No full textThis dissertation presents an integrative study of molecular and device-level engineering strategies in advanced electrochemical energy technologies, addressing key challenges across organic redox flow batteries (ORFBs), direct methanol hydrogen peroxide fuel cells (DMHPFCs), and electrochemical hydrogen pumps (EHPs). First, the influence of electrolyte pH and salt anion chemistry on redox-active organic cations (BTMAP-Fc and BTMAP-Vi) is elucidated, identifying solvent reorganizational energy (λ) as a universal descriptor for optimal electrolyte selection in ORFBs. Detailed characterization reveals that low pH methanesulfonate or chloride counterions offer superior balance of kinetic and transport properties, facilitating efficient energy storage using earth-abundant elements. Second, a modified kinetic analysis framework—adjusted Koutecky-Levich (A-K-L) equation—is developed to unravel parallel reaction pathways in the hydrogen peroxide electroreduction reaction (HPRR), surpassing the limitations of classical single-pathway models. Hydrodynamic chronocoulometry and electrode screening demonstrate that gold-based catalysts excel at selective 2-electron H2O2 reduction, providing mechanistic clarity and a practical toolkit for rapid electrocatalyst optimization toward fuel cell applications. Third, the concept of pH-gradient-enabled microscale bipolar interfaces (PMBI) is introduced for direct methanol hydrogen peroxide fuel cells (DMHPFCs), enabling simultaneous operation of alkaline and acidic environments at the anode and cathode, respectively. This configuration realizes a high theoretical open-circuit voltage (1.72 V) and quadrupled energy density compared to compressed hydrogen systems, although it also highlights the impact of mass transport limitations and membrane crossover on practical performance. This study identifies optimal anolyte and catholyte concentration, membrane thickness and flow rate to maximize the power output and minimize activation-, ohmic-and mass transfer losses. Finally, new operational protocols are proposed for low-temperature electrochemical hydrogen pumps (LT-EHPs) under CO contamination, a major barrier to hydrogen purification scalability. Advanced pulse oxidation strategies—particularly dynamic, voltage-triggered pulsing—are shown to deliver sustained catalyst regeneration, boosting separation and energy efficiency by over 10–15% compared to conventional approaches. Five-day continuous testing confirms the robustness of these methods for impurity-resilient, modular hydrogen purification. Collectively, these studies establish universally applicable molecular descriptors, introduce mechanistically precise models for complex reactions, pioneer new interface designs for fuel cell voltage and energy density enhancements, and develop resilient operational strategies for impurity mitigation in hydrogen pumps. This dissertation advances the scientific and technological foundations for next-generation sustainable electrochemical energy system
Interfacial Mineralization in Energy and Environmental Systems
No full textThe accelerating global demand for energy is intensifying energy shortages and challenging climate resilience, driven by rising CO2 emissions. Addressing these challenges requires improving energy efficiency, developing low-carbon technologies, and enabling scalable CO2 removal. This dissertation investigates two interconnected systems to advance these goals. The first examines mineral formation at liquid–liquid interfaces in enhanced energy recovery and water treatment systems, where scaling reduces energy recovery efficiency. The second explores mineralization as a dual strategy for CO2 removal and critical element recovery, with a focus on integrating carbonation and sulfidation pathways. In System 1: interfacial CaSO4 formation in enhanced energy recovery, we investigate CaSO4 nucleation and growth at oil–water interfaces. At unconfined flat oil–water interfaces, we elucidate the CaSO4 preferentially distributed at the oil–water interfaces and demonstrate that the interfacial nucleation pathway differs from nucleation in bulk solution. This new thermodynamic perspective provides strategies to better manage scaling during petroleum extraction, thereby lowering operational costs. We then extend the study to nanoscale confined water in oil emulsions, examining nucleation pathways under confinement. We further reveal how emulsion concentration influences crystallization behavior and how mineral nucleation destabilizes emulsions. In System 2: integrated CO2 removal and critical element recovery, we examine ultramafic rocks as feedstocks for integration of CO2 sequestration and recovery of critical elements, such as nickel (Ni). First, we study Ni dissolution processes from natural ultramafic rocks, low-quality ores, highlighting the role of Fe passivation in inhibiting olivine reactivity and demonstrating that reductant can enhance dissolution rates. Second, after ions are released into solutions from solid phases, we investigate coupled carbonation and sulfidation to selectively precipitate Mg as Mg-carbonate and Ni as nickel sulfide from leachates. Third, to extend the carbonation and sulfidation methods to other silicate feedstocks, we compare the reactivity of ultramafic rocks with different silicate structures to understand structural effects on carbonation and sulfidation. Fourth, to explore the influence of water flow on carbonation, we conduct experiments in natural-analog systems with flowing water and pore structures, using a microfluidic device to reveal how hydrodynamics and water transport regulate the carbonation process. Finally, to make the carbonation economically viable, we explore valorization pathways by applying carbonate coprecipitates into electrode materials, linking CO2 sequestration with value-added applications. This dissertation provides a new mechanistic understanding of mineralization processes in both natural and engineered systems. For subsurface energy recovery, it identifies strategies to control CaSO4 scaling and improve operational efficiency. For climate mitigation, it develops cost-effective pathways for CO2 removal while simultaneously recovering critical elements, and it demonstrates valorization routes that enhance economic viability. Collectively, these contributions advance a sustainable circular economy approach that links efficient energy recovery, CO2 mitigation, and resource recovery
Mitochondrial Calcium Uniporter Regulates ITAM-Dependent Platelet Activation
No full textThromboembolic conditions are the leading cause of disability and death in the United States. Platelets play an important role in the pathophysiology of thrombus formation by aiding in the formation and stabilization of the clot. Central to platelet activation is cytoplasmic calcium, which increases after platelet activation through ITAM (Immunoreceptor tyrosine-based activation motif) or GPCR (G-protein-coupled receptor) receptors. Platelet mitochondria rely on cytoplasmic calcium for mitochondrial calcium influx, which is critical for ATP formation and regulation of mitochondrial reactive oxygen species. In other cells, mitochondrial calcium entry is regulated by the multimeric protein complex, mitochondrial calcium uniporter (MCU). Deletion of MCU in other cells leads to various cellular function alterations that are cell-type dependent. In platelets, the role of MCU has not been extensively studied. Thus, determining if MCU exerts a mechanistic role in platelet function is critical for our understanding of platelet activation and thrombosis. Our study aimed to investigate the role of MCU has in platelet activation and thrombosis. Using platelet specific MCU knockout mouse on a C57BL/6 background (MCUplt-/-) as well as wildtype-littermate (MCUplt+/+) controls we demonstrated the MCU is crucial for platelet activation through the immunoreceptor tyrosine activation motif (ITAM) and that this has significant impact in-vivo thrombosis. Mice that lacked platelet MCU showed a reduction in arterial thrombosis (blood clot formation) and brain injury from ischemic stroke. To dissect the molecular mechanism by which MCU impacted thrombus formation we activated MCU KO platelets with various platelet agonists and measured the platelet response using a variety of in vitro and ex vivo techniques. The lack of MCU only affected the platelets response to ITAM receptor activation, and no other receptor, suggesting that the mitochondrial calcium entry mediated by the MCU pathway is selectively involved in ITAM specific signaling. Mechanistically we demonstrated that the MCU specific mechanism of action is through the generation of mitochondrial reactive oxygen species (ROS). ROS aids in the downstream amplification of ITAM signaling that is necessary for platelet activation. Lack of MCU decreases ROS levels leading to decrease signaling and ultimately reduced platelet activation. Interestingly similar effects were observed when human platelets were treated with MCU inhibitors, confirming the relevance of these findings to human physiology. Our results shed light on a new mechanistic pathway for platelet function and could be a target for developing new anti-platelet therapies
Studies of Seismicity in the Alaska Subduction Zone and Antarctica
No full textThis dissertation utilizes multiple methods of earthquake detection, relocation, and characterization to investigate the patterns of seismicity along the Alaska subduction zone and Antarctica. The studies of the Alaska subduction zone are built on the data collected during the Alaska Amphibious Community Seismic Experiment (AACSE) that deployed temporary land and ocean-bottom seismometers along the Alaska Peninsula and offshore regions from May 2018 to September 2019. Using seismic arrivals at those stations, as well as a combination of other land-based networks, I relocated 1307 earthquakes in the incoming plate and trench slope regions of the Alaska subduction zone with an absolute relocation technique that included a 3-D seismic velocity model. Most of the earthquakes are within 50 km of the trench in the Shumagin segment, which is consistent with the mapped locations of plate-bending faulting. I also determined the focal mechanisms of 7 earthquakes on the incoming plate using first-motion polarities of the seismic arrivals. Normal faulting earthquakes predominate the Shumagin segment, which supports the cause of the faulting as plate bending before subduction. These results suggest elevated hydration of the incoming plate in the Shumagin segment compared to other areas along strike, as well as greater potential for large, tsunamigenic earthquakes in the outer rise. In another study, I propose a new rupture scenario for the 2018 Mw 7.9 Offshore Kodiak Earthquake that occurred 300 km southeast of Kodiak Island on the incoming plate. I relocate 500 aftershocks from the 2018 Mw7.9 Offshore Kodiak Earthquake using a relative relocation technique that solves for the location of the center of all of the events and the locations of events from that center. The locations of the events indicate three main north-south clusters of events, with the central cluster including the mainshock. There are many other, smaller north-south clusters of events interspersed between the main clusters, highlighting a southwest to northeast trend of en echelon-style faulting. High-resolution bathymetry and sub-bottom profiles show north-south faulting is pervasive across the aftershock region, with offsets in the subsurface reflectors indicating these faults have slipped repeatedly. I also find that the Coulomb stress increased along north-south faults from the mainshock rupture when modeling the stress change. I propose a new rupture scenario for the 2018 Mw 7.9 Offshore Kodiak Earthquake wherein many north-south en echelon faults ruptured following the mainshock. In the final study, I create a catalog of regional seismicity across sparsely-instrumented regions of Antarctica using a novel, deep-neural-network-based phase picker (autopicker). Existing catalogs of seismicity across Antarctica miss large regions that are distant from seismic stations. I train a new autopicker focused on regional arrival detection with manually-reviewed, high-quality seismic arrivals at Antarctica stations. I find 4246 events for 5 years, 2009-2013, of data. The seismicity is mostly concentrated in the Transantarctic Mountains, Marie Byrd Land, the Gamburtsev Mountains, and around coastal glaciers like Thwaites and Totten. These areas are prone to several seismic sources, including tectonic faulting, volcanism, and glacial movement. My catalog covers most of Antarctica and indicates promise in expanding the work to more years of data
Interference Management For Next-Generation Dynamic Spectrum Sharing
Get PDFThe exponential growth of wireless devices and bandwidth-intensive applications has intensified the demand for efficient spectrum utilization, exposing the limitations of traditional static spectrum allocation schemes. Next-generation spectrum sharing has emerged as a transformative solution to enhance spectrum efficiency by enabling multiple wireless systems to coexist opportunistically in the same frequency band and geographic area. However, such dynamism introduces significant challenges, particularly in interference management, which is critical to enabling reliable coexistence, ensuring access priority, and building mutual trust across diverse applications. This thesis advances interference management by developing advanced techniques for interference prediction, monitoring, and control in dynamic spectrum sharing environments. Key contributions include the Channel Estimation via Loss Field (CELF) model for accurate and rapid channel loss prediction, the augmented CELF model to enhance explainability and robustness under uncertainty, and a Full-Duplex spectrum Monitoring system (FDMonitor) developed and deployed on experimental testbeds. The CELF work uses channel loss measurements from a deployed network area and a Bayesian linear regression method to estimate a site-specific loss field for the area. Real-world indoor and outdoor datasets validate that CELF is more accurate than common machine learning (ML) benchmarks and is less computationally complex to train. A continued work on CELF explores different base models and spatial multipath effects for the modeling components in CELF. It also verifies analytically and numerically the explainability of CELF, and validates its robust performance in complex environments. The FDMonitor system uses a bidirectional coupler, a two-port receiver, and a new source separation algorithm to simultaneously and adaptively estimate the transmitted signal and the signal incident on the antenna. FDMonitor has been running on POWDER, a large-scale wireless experimental testbed, since 2021, monitoring 19 SDR platforms accessible by outside experimenters. Results show that it achieves a low false alarm rate over 27 months of operation. Together, these solutions—supported by statistical models and extensive experimental validation—offer scalable, efficient, and trustworthy interference management strategies to enhance spectrum efficiency and boost openness in wireless applications like radio dynamic zones and private cellular networks
Targeting Cyst(e)ine Dependence and Redox Metabolism in Genetically Distinct Sarcomas
No full textRewiring of cellular metabolism is a well-established hallmark of cancer biology. Cancer cells alter metabolism to support the bioenergetic, biosynthetic, and redox demands of malignant transformation. Cancers vary widely in the substrates and pathways utilized for biomass and energy production. These variations can arise from tissue of origin, tumor driving mutations, and tumor microenvironment pressures. However, highly proliferative tumors share the need to neutralize the reactive oxygen species (ROS) generated by their enhanced metabolic demands. Increased demand for ATP production and biomass production in cancer cells drives increased ROS production in the mitochondria, peroxisomes, endoplasmic reticulum, and other cellular compartments. Therefore, elevated ROS burden relative to normal tissues is prominent is a feature of cancer metabolism. While a baseline level of ROS is necessary for cellular signaling, elevated ROS levels that overwhelm the neutralization capacity of cellular antioxidant systems result in oxidative stress including DNA oxidation, deleterious protein oxidation, and oxidation of lipid membranes. To maintain redox homeostasis, cancer cells exhibit alterations in metabolism to support critical cellular antioxidant systems. Elevated ROS burden and compensatory increased dependency on cellular antioxidant systems make targeting redox metabolism a promising strategy for therapeutic development. The glutathione antioxidant system and the thioredoxin antioxidant system are the two primary cellular antioxidant systems necessary for the maintenance of redox homeostasis in cancer cells. Glutathione (GSH) is the most abundant intracellular antioxidant and is synthesized from glutamate, glycine, and cysteine to form the GSH tripeptide. GSH functions as a reductive co-factor for glutathione peroxidases (GPXs) and glutathione transferases (GSTs) to neutralize hydrogen peroxides, lipid peroxides, and other ROS. Utilization of GSH as a co-factor for ROS neutralization results in oxidation of GSH to form GSSG. GSSG is recycled to GSH by glutathione reductase (GR) in an NADPH dependent process. The thioredoxin system uses thioredoxin (Trx), a small protein antioxidant with a conserved cysteine moiety in the catalytic domain, as the central reductive component. Thioredoxins reduce peroxiredoxins and other redox active proteins to maintain their redox functions, resulting in thioredoxin oxidation. Thioredoxins are recycled to a reduced state by thioredoxin reductase (TrxR) in an NADPH dependent process. The glutathione and thioredoxin systems share many ROS substrates, resulting in considerable overlap between the two antioxidant systems. Dependency upon the glutathione antioxidant system and the thioredoxin antioxidant system vary between cancer subtypes and at different stages of tumor progression. However, dependency upon NADPH production and cysteine are shared between the two systems. As a result, targeting ROS homeostasis through inhibition of NADPH production or cysteine metabolism are emerging mechanisms for therapeutic development in cancer. In particular, interest in inhibiting cysteine metabolism in cancer cells has been growing since the discovery of ferroptosis, a distinct ROS mediated form of programed cell death. Although cysteine is a non-essential amino acid in most normal body tissues, cysteine becomes essential in many cancers due to increased dependence upon intracellular cysteine pools to maintain ROS homeostasis. While cells can synthesize cysteine through the transsulfuration pathway, recent studies suggest that most cancers are dependent upon cystine import through system xCT. The cystine-glutamate anti-porter, system xCT, is over expressed in many cancer subtypes. Additionally, inhibition of xCT or extracellular cystine depravation have been shown to induce ferroptosis in a variety of different cancer subtypes in vitro and in vivo including but not limited to lung cancer, pancreatic cancer, and breast cancer. However, not all cancers are sensitized to xCT inhibition at baseline and metabolically targeted drugs frequently fail in clinical trials when given as a single agent due to the expansive metabolic flexibility of cancer cells. Therefore, research characterizing sensitivity and combinatorial treatment strategies is important for clinical translation of pharmacological xCT inhibition. Alterations in gene expression for key enzymes in redox metabolism or transcription factors regulating antioxidant systems have been used as biomarkers to predict sensitivity to redox metabolism-based cancer therapeutics. Therefore, we used unbiased screening to identify alterations in metabolic gene expression in a diverse group of sarcomas. We identified two sarcoma subtypes, synovial sarcoma (a translocation driven soft tissue sarcoma) and osteosarcoma (a bone sarcoma of complex etiology), that exhibit unique metabolic changes that sensitize them to perturbations of redox metabolism. The first research aim focused on the elucidation of redox metabolism in synovial sarcoma (SS). Screening of gene expression in SS patient samples revealed significantly reduced expression of malic enzyme 1 (ME1). ME1 absence was confirmed in SS patient tissue samples by IHC and in human SS cell lines and mouse tumor models of SS by qPCR and protein expression analysis. ME1 is a cytosolic enzyme that catalyzes the reductive carboxylation of malate to pyruvate producing CO2 and NADPH in the process. ME1 contributes to the cytoplasmic NADPH pool along with enzymes in the oxidative pentose phosphate pathway (oxPPP) and IDH1. Targeted tracing of glucose metabolism in ME1-null WT SS cell lines and ME1 overexpressing (OE) control cell lines revealed increased flux through the pentose phosphate pathway (PPP) in ME1-null SS. Inhibition of the oxPPP with G6PD-i revealed that flux through the oxPPP was necessary in ME1-null WT SS to maintain intracellular NADPH levels for cell survival. Consistently, ME1-null WT SS exhibited reduced GSH/GSSG ratios compared to ME1-OE SS controls. Small molecule inhibitors of the glutathione antioxidant pathway (BSO) and the thioredoxin antioxidant pathway (D9) demonstrated a shift in dependence from the GSH pathway to the thioredoxin pathway in ME1-null SS. Metabolomics revealed reduced intracellular cysteine levels in ME1-null WT SS relative to ME1-OE SS controls, suggesting increased cysteine demand in the context of ME1 absence. To target the intrinsic redox metabolism of ME1-null SS we utilized small molecule inhibitors of cystine import through system xCT (erastin and ACXT-3012) in ME1-null SS and ME1-OE controls. ME1 null SS were sensitized to xCT inhibition both in vitro and in vivo. xCT inhibition in vitro with erastin resulted in significant increases in lipid peroxidation and induction of cell death via ferroptosis. In vivo inhibition of xCT with ACXT-3012 resulted in tumor control in ME1-null SS xenografts but had no effect on tumor growth in ME1-OE control xenografts. Collectively these data demonstrate that absence of ME1 in SS results in significant alterations to redox metabolism that potentiate cell death with inhibition of cystine import through system xCT. Similar unbiased screening methods in osteosarcoma recently revealed that PHGDH overexpression in osteosarcoma patient samples is a recurrent metabolic feature that correlates with significantly worse patient prognosis. PHGDH is the rate limiting enzyme in the de novo serine synthesis pathway, which has been linked to mitochondrial NADPH production and redox homeostasis in cancers and endothelial tissues. Therefore, the second research aim sought to evaluate the contribution of de novo serine synthesis to redox homeostasis in osteosarcoma. Unbiased screening of whole metabolomic data revealed significant reductions in GSH/GSSG ratios upon inhibition of PHGDH in osteosarcoma cell lines. Characterization of ROS levels in osteosarcoma cell lines treated with NCT-503, a small molecular inhibitor of PHGDH, revealed significant accumulation of mitochondrial ROS. Collectively, these data suggest that de novo serine synthesis is necessary for redox homeostasis in osteosarcoma. Serine can contribute to GSH synthesis by functioning as a substrate for cysteine synthesis through the transsulfuration pathway. Upon PHGDH inhibition intracellular serine levels were reduced while other substrates of the transsulfuration pathway accumulated and cysteine levels were reduced. These data collectively suggest reduced activity of the transsulfuration pathway. Consistently, U13C6-glucose tracing demonstrated that PHGDH inhibition halted glucose contribution to GSH synthesis in osteosarcoma cell lines. While PHGDH inhibition in osteosarcoma results in oxidative stress and reduced proliferation it does not induce cell death. To identify compensatory mechanisms promoting cell survival with PHGDH inhibition in osteosarcoma, mRNA screening of a panel of metabolism genes was conducted. Inhibition of PHGDH resulted in significantly increased expression of SLC7A11, the cystine-glutamate antiporter of system xCT. Consistently, treatment with PHGDH induced increased cystine import in osteosarcoma and increased xCT plasma membrane expression. We hypothesized that PHGDH inhibition increased dependency upon exogenous cystine import through xCT. Consistent with this hypothesis, treatment with NCT-503 significantly increased sensitivity to xCT inhibition in vitro resulting in significant cell death in physiologic conditions. Taken together these research aims highlight a powerful approach for the development of targeted therapeutics based on redox metabolism in sarcoma. In SS and osteosarcoma, two genetically diverse sarcoma subtypes that share few genetic features, unbiased screening revealed distinct metabolic changes that induced sensitivity to redox perturbations. Through detailed metabolic characterization it was demonstrated that ME1 absence in SS and PHGDH inhibition in osteosarcoma function through desperate mechanisms to sensitize both cancers to inhibition of cystine import. This work identifies novel opportunities for translational development in both SS and osteosarcoma through xCT inhibition. Additionally, this work suggests a pipe-line approach of unbiased screening, metabolic characterization, and pharmacological targeting to be applied to other sarcoma subtypes for further exploration of redox metabolism and therapeutic development in sarcoma
Sitting with Wounds: The Visual Poetics of Grief in Charlotte Salomon’s Graphic Life Narrative Life? or Theater?
No full textThis dissertation investigates the role of grief in the visual text Leben? oder Theater? Ein Singespiel (Life? or Theater? A Musical Opera) produced by the German-Jewish artist Charlotte Salomon in hiding from the Nazis between 1941 and 1942. In this autobiographical material, consisting of a collection of over 700 gouache paintings that come with an accompanying script, Salomon creates a visual language for mourning and suffering related to the familial history of Jewish women’s suicides alongside the artist’s experience of displacement amidst the period of the Holocaust. My study traces the facets of Salomon’s multiperspectival visual storytelling in which the artist transforms grief and trauma into a creative language. My survey shows how this transformation can be regarded as a mourning practice enabled through aesthetic production. The study is incited by the following questions: How can we better understand the interrelationship between grief, gender, displacement, and aesthetic practice? How does the artist negotiate her human right to mourn in a period of ongoing loss under the threat of persecution? Drawing from contemporary autobiography theory, I argue that Salomon produced her work out of an impulse to not only preserve a life story amidst the threat of its obliteration but also to establish her artistic legacy. By analyzing both image and text in their intermedial interplay, I illuminate both the narrative and visual strategies that Salomon employs to tell her story. Doing so, I combine perspectives from cultural theory and literary theory that put Salomon’s idiosyncratic artwork into a new light and enhances our reading of it. Using the concept of life writing, each chapter investigates the visual narrative strategies with which the artist forms a story that gives testimony to and materializes an archive about the history of Jewish women’s suffering and grief that thwarts both the discursive and familial elision of this reality. With its focus on the performative facets of the narrative voices as well as the multifaceted textures of grief this study presents not only a new intervention into the Salomon scholarship but also into current discourses on the meaning of aesthetic production amidst ongoing crises. Scholarship on Charlotte Salomon has to date been situated primarily within art history and literary studies. This interdisciplinary study bridges fields, foregrounding auto/biography theory as its principal approach while simultaneously contributing to ongoing conversations in German Studies, Jewish Studies, art history, and exile studies