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Renaissance 21

Renaissance 21 will run a 10-week after school program at Garfield Teen Life Center located at 428 23rd Avenue. The program will train 10-12 youth to develop mobile and desktop websites. In addition to paid instructors, STEM professionals, college, and high school volunteers will serve as mentors to the program participants. This project will be completed by January 31, 2020.

Renaissance 21

Renaissance 21 will pilot a 10-week after school program that will train 10 youth to develop mobile/desktop game and website applications. STEM professional, college, and high school volunteers will also serve as mentors to the program participants.

NIMH - National Institute of Mental Health

Human brain rhythms serve as representations of inner states of the brain for vigilance and behavior. Dysregulation of brain rhythms is implicated in most neuropsychiatric and neurodegenerative disorders. The molecular, cellular, and circuit mechanisms underlying mammal brain rhythms have been mainly elucidated in animal models. However, the lack of tractable model has challenged the investigation in human system. We have developed methods to produce the 3D structures representing the human cortical (hCO, human cortical organoids) and thalamic (hThO, human thalamic organoids) areas by applying stem cell technologies. These organoids reproduce the developing and functional human brain. Most recently, we generated ventralized thalamic organoids (vThOs) that contain interneurons that are specifically present in thalamic reticular nucleus (TRN). The fusion or assembly of two or more neural organoids have shown the possibilities to study the interaction of the brain domains. While many previous studies have successfully demonstrated the utility of human brain organoids in modeling diseases, no studies have developed human brain organoids that reproduce human brain rhythms. The neuronal connection between thalamus and cortex are crucial for the formation of human cortical oscillations commonly observed in scalp EEG. Thus, our established hCOs and ThOs are essential elements to produce the cortical oscillations. Here, we will assemble the organoids to test the hypothesis that assembloid of hThO and vThO together with hCO generate thalamocortical oscillations via a synaptic interaction among these functionally distinct organoids. In Aim 1, we will develop hThO-vThO assembloids to produce intrinsic thalamic network oscillations. We will examine the role of TRN GABAergic cells in intrinsic thalamic network oscillations. In Aim 2. we will develop methods to produce hCOs assembled with hThO-vThO thalamic assembloid to generate thalamocortical network oscillations. Here, we will develop a thalamocortical network oscillation that reproduces human cortical rhythms. In Aim 3, we will test effect of the noradrenaline and acetylcholine on thalamocortical oscillation formation by examining the neural gene regulation, cellular and synaptic properties of thalamic neurons, and development of thalamocortical network activity. The results will define molecular, cellular, and circuit mechanisms of how neuromodulators promote proper thalamocortical network oscillation development. Overall, our project will generate the assembloids of cortical and thalamic organoids to reproduce the human corticothalamic oscillation, and will offer a highly innovative platform to define the molecular and cellular underpinnings of human cortical oscillation and its associated diseases.

NIA - National Institute on Aging

Myelodysplastic Syndromes (MDS) are a group of bone marrow failure disorders caused by clonal expansion of hematopoietic stem cells (HSC) that fail to produce mature blood cells of sufficient quality and quantity. The disease-causing HSC bear acquired mutations that confer a selective advantage compared to other HSC but are detrimental to hematopoiesis. Typically, the mutations confer increased proliferation and survival upon HSC and their progeny, creating a hypercellular bone marrow with increased proportions of immature myeloid cells. In contrast, mutations in DDX41, an essential RNA helicase, cause reduced proliferation and survival of hematopoietic progenitors and yet contribute to about 4% of MDS cases. DDX41-mutated MDS most often occurs in individuals with inherited heterozygous mutations in the gene, 50-70% of which are truncating (frameshift or loss of translation start) and are thus considered loss-of-function. The other 30-50% of these are missense mutations, whose effect on protein function is largely unknown. The most common acquired mutation occurring in these patients is a second-hit mutation affecting the other allele of DDX41, typically causing the amino acid change R525H. Unique features of DDX41-mutated MDS include a hypocellular bone marrow, few co-mutations, and relatively slower disease progression. Our published and preliminary data indicate that the most common combination of DDX41 mutations observed in patients (truncating/R525H) causes a profound defect in hematopoietic progenitor cell proliferation and survival. Remarkably, our patient sequencing studies demonstrate that HSC bearing biallelic DDX41 mutations clonally expand and dominate the HSC pool, accounting for over 90% of HSCs in 11 out of 11 patients analyzed but only 5-25% of total bone marrow cells. These data and our published mouse models indicate that biallelic DDX41 mutations are favored in HSC but strongly detrimental to progenitor cells. Mechanistically, we found that DDX41 is required for ribosome biogenesis through its function in splicing at small nucleolar RNA (snoRNA) genes. Thus, biallelic DDX41 mutations confer reduced protein synthesis, which is a cause of the progenitor cell viability defect. HSC maintain a lower protein synthesis rate than progenitors, even when cycling, likely for protection from proteotoxic stress, which contributes to aging-associated decline of HSC and other tissue-specific stem cells. We hypothesize that biallelic DDX41 mutations are positively selected in aging HSC pools due to a reduction in proteotoxic stress. In the case of germline missense mutations, this requires dominant negative effects by the acquired R525H mutation to cause reduced protein synthesis and the associated stem cell expansion and progenitor cell defect. To test these hypotheses, we propose to determine the effect of combined germline and acquired missense DDX41 mutations on HSC function through analysis of MDS patient samples and mouse models, and then we propose to determine if proteotoxic stress is the driver of the clonal advantage of biallelic DDX41-mutated HSC in aging bone marrow through analysis of genetically and temporally precise mouse models of the disease.

NIAID - National Institute of Allergy and Infectious Diseases

Summary T cells are central to transplant rejection, driving allograft destruction through differentiation into effector cells. However, the mechanisms by which effector T cells sustain persistent alloimmune responses remain unclear. Our recent studies have identified a subset of “stem-like” T cells within the alloreactive pool. These stem-like T cells possess two fundamental features: self-renewal and the capacity for continuous differentiation into effector T cells. Importantly, terminal effector T cells, despite having all the cardinal features of effector activity, rapidly undergo apoptosis and fail to sustain graft rejection in vivo. This underscores the critical role of stem-like T cells, which continuously generate effector T cells to drive allograft rejection. Understanding the fundamental mechanisms regulating T cell stemness is a key question with significant therapeutic implications. Our preliminary data reveal that T cell stemness is epigenetically regulated by enhancer of zeste homolog 2 (EZH2), the catalytic subunit of the Polycomb Repressive Complex 2 (PRC2). EZH2 functions as a histone methyltransferase, catalyzing the trimethylation of histone H3 at lysine 27 (H3K27me3), a key marker of gene repression. Deletion of Ezh2 in T cells completely abrogates their differentiation into effector cells. Furthermore, mice with T cell-specific EZH2 deletion (Ezh2fl/flCd4-Cre) or WT mice transiently treated with an EZH2 inhibitor (DZNep) accepted heart allografts long term (>100 days). These results suggest that EZH2 deletion/inhibition disrupts the stemness of alloreactive T cells, rendering them unable to sustain graft rejection. The central goal of this proposal is to elucidate how EZH2, an epigenetic repressor, regulates T cell stemness. We hypothesize that EZH2 preserves two key features of stem-like T cells: maintaining their long-term functional persistence and enabling their differentiation into effector cells. This hypothesis will be tested through two aims: Aim 1: Investigate whether EZH2-mediated repression of key transcription regulators is required for the differentiation of stem-like T cells into effector cells. Aim 2: Investigate whether EZH2 preserves T cell stemness by epigenetically repressing genes involved in apoptosis, cell cycle arrest, and functional exhaustion. Successful completion of these studies will uncover the epigenetic mechanisms governing stem-like T cell persistence and effector differentiation, providing a foundation for novel therapeutic strategies to improve transplant outcomes.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Clostridioides difficile infection (CDI) poses a significant public health burden, with approximately half a million cases annually in the United States and recurrence rates of up to 25%. CDI is primarily driven by disruptions to the gut microbiome, often due to antibiotic treatment, which creates an environment conducive to C. difficile (Cd) colonization. Current microbiome-based therapeutic strategies, such as fecal microbiota transplants (FMTs), have shown promise in restoring colonization resistance; however, their safety, reproducibility, and regulatory challenges limit widespread clinical application. While defined microbial consortia represent a promising alternative, their efficacy remains suboptimal. We hypothesize that these failures stem at least in part from an over-reliance on high-abundance (HA) species and an incomplete understanding of how low- abundance (LA) species contribute to microbiome stability and pathogen resistance. This project seeks to systematically evaluate the role of LA species in microbiome assembly and in conferring colonization resistance using a combination of synthetic microbial communities, metabolomics, and gnotobiotic mouse models. We hypothesize that LA species play crucial metabolic and ecological roles, through direct competition with Cd and by reinforcing community resilience under antibiotic-induced perturbations. To test this hypothesis, we will employ a defined yet complex synthetic community, mhCom, that encompasses both HA and LA species and assembles reproducibly in vitro and in vivo. Leveraging high-resolution metabolomics, we will (i) characterize the metabolic niches and functional redundancies of LA species and (ii) determine their role in resistance to Cd colonization and microbiome recovery and Cd suppression following antibiotic-induced CDI. In Aim 1, we will map the metabolic functions of LA species within mhCom in vitro, identifying privileged metabolic niches and cross-feeding interactions that contribute to community stability. We will use untargeted metabolomics and species dropouts to establish whether LA species and/or Cd fill metabolic voids when HA species are lost. In Aim 2, we will use gnotobiotic mice to assess the impact of LA species on C. difficile colonization resistance, determining whether the inclusion of LA species enhances pathogen exclusion both before and after antibiotic-induced microbiome disruption. By addressing a critical knowledge gap in microbiome ecology, this study has the potential to redefine microbiome-based therapeutics, either by demonstrating that LA species are not merely passive members of the gut community but essential contributors to microbiome resilience or by affirming strategies focused on HA species. The outcomes of this research will inform the rational design of next-generation microbial therapeutics with enhanced robustness against CDI and will have direct impact for other microbiome-related diseases, providing a foundation for safer, more effective, and precision-targeted microbiome interventions.

NCI - National Cancer Institute

Abstract The ability of tumor cells to adapt and survive endogenous and environmental stress is essential for tumor initiation and development. Glioblastoma (GBM) is the most malignant brain tumor, with high mortality and resistance to therapy. Within the heterogeneous GBM tumors, a highly tumorigenic subpopulation of Glioma Stem Cells (GSCs) drives tumor growth and promotes recurrence. GSCs can survive and proliferate in a relatively hostile tumor microenvironment, which triggers adaptive stress response mechanisms to restore protein homeostasis and promote tumor cell survival under abnormal conditions. Most forms of stress converge on one signaling pathway termed the integrated stress response (ISR), which signals through phosphorylating eIF2α (p-eIF2α; eukaryotic translation initiation factor 2α). Activation of the ISR causes a temporary shutdown of global protein translation and selective translation of cytoprotective transcripts. However, under prolonged stress, p-eIF2α promotes apoptosis. p-eIF2α halts protein synthesis by inhibiting eIF2B, which plays a key role in regulating mRNA translation and balancing the pro- and anti-survival effects of p-eIF2α. Our studies revealed a direct link between ISR signaling and response to several GBM therapeutics. Our central hypothesis is that the interplay between p-eIF2α and eIF2B determines therapeutic sensitivity and translation potential that drives tumor growth. We propose that while high levels of ISR effectively block global protein translation, mild ISR signaling, such as one caused by therapy, reprograms translation and selectively enhances the translation of a subset of mRNAs to confer cytoprotection and promote survival. To test our hypotheses and to address how conventional GBM therapies or the abnormal tumor microenvironment supports tumor progression and confers therapeutic resistance, we propose to carry out the following aims: Aim 1. Defining the role of eIF2B in translational regulation, tumor growth, and therapy response. Aim 2. Investigating the role and mechanism of translational reprogramming in GBM therapy response. Aim 3. Selective Targeting of aminoacyl-tRNA synthetases to enhance the efficacy of GBM Therapies. The proposed work will determine whether modulating the ISR could impair tumor growth and increase the efficacy of targeted therapeutics currently used in the clinic. Cell culture or in silico models cannot closely mimic the tumor environment, compounds pharmacokinetics and brain penetrance of small molecules, therefore the use of animals is warranted in our study.

NINDS - National Institute of Neurological Disorders and Stroke

Project Summary The incidence of stroke increases in women after their menopause, and stroke outcomes also become worse with aging in female stroke patients. It has been hypothesized that the exacerbated stroke phenotypes seen in elderly women are due to the loss of E2’s neuroprotection after menopause; however, the Women’s Health Initiative trial (WHI) has found E2 replacement therapy (ERT) had detrimental effects on stroke. Stroke scientists have argued that the women involved in the WHI trial were well passed their menopause when they received the ERT (late ERT or lERT), and have now shown ERT administered early after the menopause (early ERT or eERT) confers neuroprotection. Interestingly, for the past decade the increasing data have suggested that the second X chromosome (chromosomal effect) contributes to the worsened stroke outcomes in elderly women in addition to the decline of E2 levels (hormonal effect). Specifically, the X chromosome linked gene Kdm6a that escapes from X chromosome inactivation (XCI) in microglia has been found to up-regulate the histone H3K27me1 activational effect on the transcription of the pro-inflammatory IRF5 (interferon regulatory factor 5; responsible for microglial pro-inflammatory activation), leading to exacerbated stroke outcomes. In this proposal, we hypothesize that eERT in postmenopausal females inhibits Kdm6a gene escape from XCI, and suppresses the Kdm6a-H3K27-IRF5 signaling to ameliorate post-stroke inflammation and improve stroke outcomes. Aim 1 will use aged WT mice (in vivo) and in vitro assays (human induced pluripotent stem cells, hiPSCs), and test the hypothesis that the escape of Kdm6a from XCI and the Kdm6a-IRF5 signaling in aged females are repressed by eERT; whereas lERT will not have the same effects. Aim 2 will Test the hypothesis that eERT’s effect on post-stroke inflammation and outcomes is not Kdm6a allele dosage dependent but lERT's is. Microglial and astrocytic Kdm6a conditional knockout (CKO) female mouse models will be used to produce the knockout of one allele of Kdm6a in these cells. Kdm6a floxed females (two alleles of Kdm6a) will be included as a comparison. Aim 3 will examine if surgical menopause promotes Kdm6a escape from XCI in microglia. Ovariectomy will be performed in young and adult female mice to generate surgical menopause model. Kdm6a escape from XCI, Kdm6a-H3K27-IRF5 signaling, post-stroke inflammation and outcomes will be investigated in Aim 3. The goal of this project is to target XCI gene escape to suppress neuroinflammation after stroke.

NCI - National Cancer Institute

Project Summary Since 1990, the biennial International Workshop on Molecular Aspects of Myeloid Stem Cell Development and Leukemia has been the premier global meeting which spans fundamental stem cell biology and function, myeloid cell differentiation, marrow failure syndromes and myeloid cell malignancies. At the 2026 installment of the meeting (“MYELOID2026”), scientists with expertise in normal and abnormal hematopoiesis and clinicians who treat patients with myeloid leukemias, malignancies, and pre-leukemic disorders and also have active research programs in these diseases will achieve a better understanding of critical steps/factors that regulate hematopoiesis, their impact on transformation and disease resistance, and their potential relevance in clinical settings. MYELOID2026 will stimulate the community with collaborations on active projects, educate trainees, and “cross pollinate” critical and influential sectors of multiple myeloid biology fields. Moreover, the meeting size, meeting program, and ratio of trainees to faculty at the MYELOID meetings, provide trainee attendees ample opportunities for networking and faculty engagement for project discussions. We expect several landmark studies for the respective fields of normal hematopoiesis, stem cell biology, and myeloid malignancies to result from presentations by attendees. MYELOID2026 will bring together world renowned scientists, clinicians, and trainees to improve our understanding of hematopoietic development and differentiation, stem cells, and the evolution of myeloid malignancies.

NCI - National Cancer Institute

PROJECT SUMMARY/ABSTRACT No changes are being made in this proposed supplement to the stated project summary. With the evolution of the Experimental Therapeutics Clinical Trials Network (ETCTN), the Johns Hopkins Translational Science Team (JHTST) supports 8 Affiliate Organizations (AO) under our Lead Academic Organization (LAO) with the goal to enhance and accelerate our collective contribution to the drug development efforts of the NCI. We have organized a comprehensive and cohesive infrastructure that can conduct high-quality clinical trials evaluating novel anticancer agents, in combinations, in molecularly selected patient populations, or rare tumor sites. Our infrastructure stems from the need to be clinically efficient, regulatory compliant and scientifically rigorous in our approach as we collaborate as network members within the ETCTN. Our infrastructure consists of seven experienced NCI-designated Cancer Centers: Johns Hopkins Sidney Kimmel Comprehensive Cancer Center, Emory Winship Cancer Institute, Georgetown Lombardi Comprehensive Cancer Center, Sidney Kimmel Cancer Center at Thomas Jefferson University (withdrawn), Memorial Sloan Kettering Cancer Center, University of Virginia Cancer Center, University of Wisconsin Carbone Cancer Center, University of Colorado Denver, University of Maryland Greenbaum Cancer Center, and most recently Wake Forest University. This collection of Centers brings together many unique discovery strengths, diverse patient volumes, and locations both urban and rural. We will focus on 4 specific aims: Aim 1- To lead and maintain a clinical trial consortium that will support cancer clinical trials from Phase 1 initiation through proof-of-activity and foster seamless Phase 2 clinical development of NCI CTEP IND agents; Aim 2- To actively participate and engage disease-focused clinical investigators in the ETCTN by promoting accrual to a range of ETCTN studies led by other LAO/AO members; Aim 3- To incorporate and implement innovative correlative and biological laboratory studies in the context of or as eligibility for participation in early phase clinical studies that enhance our understanding of determinants of toxicity and response that will be used for further definitive practice-changing clinical trial evaluation; and Aim 4- To train the next generation of investigators in drug development. With 9 centers within our consortium, we anticipate no problem in meeting the grant metrics of 100 accruals per year, submitting enough LOI concepts to have 6 new studies approved each year, functioning as a network by having Disease-Focused Clinical Investigators champion ETCTN studies at each site across disease sites, and to provide opportunities to engage and train early career investigators in drug development. We anticipate that our contributions within the ETCTN will impact the clinical care of cancer patients.

NIAMS - National Institute of Arthritis and Musculoskeletal and Skin Diseases

ABSTRACT Systemic autoimmune diseases such as systemic lupus erythematosus (SLE) are mediated by autoantibodies against key tissue constituents, accompanied by the activation of innate immune system. In addition, systemic autoimmunity is frequently associated with hematological complications such as lymphopenia, anemia and/or thrombocytopenia, which can be debilitating and even life-threatening. These abnormalities are typically considered as isolated symptoms caused by autoantibodies against the respective blood cell types, and are treated by immunosuppressive therapies. On the other hand, it is possible that frequent hematopoietic abnormalities in SLE may reflect a defect in the source of hematopoiesis, i.e. hematopoietic stem cells (HSC) and/or progenitors. This model has important implications for the pathogenesis and treatment of SLE; however, it remains to be supported by genetic and mechanistic evidence. Our preliminary studies suggest that the bone marrow from mice with SLE-like disease showed impaired ability to reconstitute irradiated recipients. Moreover, HSCs in moribund mice showed increased proliferation and upregulation of transcripts associated with stem cell exhaustion. We therefore hypothesize that clinical SLE-like disease impairs the activity of HSC, which may further exacerbate hematological abnormalities and inflammation. This hypothesis will be tested using two Specific Aims. In Aim 1, we will characterize HSC impairment in a mouse model of SLE-like disease, including its cell-extrinsic nature and relevance to endogenous hematopoiesis. In Aim 2, we will characterize the epigenome of disease-affected HSC, as well as molecular pathways that cause HSC impairment in this model. Collectively, these studies may support the paradigm of impaired HSC activity as a source of hematopoietic abnormalities and "trained autoimmunity" in SLE. As such, they may pave the way for future studies of stem/progenitor function in human SLE and of its potential therapeutic modulation.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The National Summer Undergraduate Research Project (NSURP) was created as an eight-week virtual summer research program in the microbial sciences that matches underrepresented minorities in STEM undergraduate students nationwide with faculty mentors worldwide to address the barriers presented by COVID-19 cancelations. NSURP mentees conduct research from any location with an internet connection, allowing students to learn how to conduct impactful research by forming and testing hypotheses. As individuals returned to in-person programs, NSURP found a population unable to travel, independent of COVID-19, due to financial, familial, geography, and health constraints. As we see an increased demand from these individuals, post-pandemic, who can’t travel to in-person opportunities, we seek to expand our ability to serve these undergraduates with research opportunities in our program and provide them with year-long mentoring and professional development. NSURP seeks to apply its virtual research model to human health-related topics, such as the basic and applied disease research conducted within the purview of the NIAID, both in microbiology and immunology. Implementing NSURP within the NIAID infrastructure will create more opportunities for URM scientists and ultimately aid in developing a diverse biomedical research workforce. The central premise of NSURP is to meet undergraduates where they are, facilitate exposure and pursuit of a scientific opportunity, and give them the tools and confidence to continue in their scientific careers. To maximize the contribution of NSURP within the NIAID mission, we will 1) provide virtual biomedical-specific summer research opportunities within the NIAID mission for minoritized undergraduates, 2) facilitate synergistic virtual scientific and career multi-level mentoring relationships, and 3) assess program impact by evaluating educational outcomes of NSURP participants and conducting longitudinal studies on the effects of culturally-responsive virtual mentorship training.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Infectious stress and damage are important concepts; however, we still lack understanding of how immunity and microbial virulence result in cellular stress, and how this stress in turn influences the immune response. Using a powerful model system, Drosophila melanogaster, we have recently found that phosphorylation of histone H2a (γH2av) is a hallmark of microbial infection (oral infection, septic injury). γH2av is considered a marker of DNA damage response (DDR) downstream of DDR kinases (ATM, ATR, DNA-PKc). We found that pathogens induce host γH2av accumulation in a virulence-, NOX- and ATM kinase-dependent manner, but without DNA damage. We have also found that ATM-mediated signaling promotes inflammatory cytokine production, alters cell dynamics and strongly promotes survival to infection. Based on these results, we hypothesize that ATM- mediated signaling is a central stress response upon infection, altering cytokine production and modulating cell death and survival. To test these hypotheses, we propose the following specific aims: Aim1: We will determine the microbial characteristics (immunogenicity, virulence/tissue damage) that induce γH2av accumulation in midgut enterocytes (ECs). In parallel, we will analyze the role of NADPH oxidases (Duox, NOX) on triggering the ATM pathway. Finally, we will elucidate how cellular age influences the ability of a cell to trigger ATM signaling upon infection. Aim2: We will analyze the impact of ATM signaling in enterocytes where it regulates inflammatory cytokine production, cell dynamics and tissue repair. We will clarify the cell-autonomous requirement of ATM signaling for enterocyte elimination, cytokine induction and tissue repair using a combination of FACS, RNA sequencing, functional genetics, cell tracing and pharmacological treatments. Aim3: We will investigate how ATM signaling decreases host survival upon septic injury. We will first elucidate and characterize spatial-temporal activation of ATM signaling in response to systemic infection and identify key regulators involved. We will determine the mechanisms leading to host lethality downstream of ATM signaling. Finally, we will investigate whether γH2av itself mediates some of the influence of ATM signaling upon infection. This project will demonstrate that NOX-ATM signaling acts as a new central regulator of infectious stress and immunity. Our multi-omics approach coupled with tissue-specific functional genetics and unparalleled Drosophila lineage tracing and clonal systems will help clarify both the upstream regulators and downstream effects of this pathway. Importantly, our work will also show how a stress response can increase or decrease survival to infection in different tissue and infection contexts. We will demonstrate that NOX-ATM is not only central for the control of cytokine production and innate immunity, but also a key regulator of cell death and stem cell-mediated repair. Finally, our research may open new avenues of research on cellular aging and immune stress responsiveness. The key characteristics by which pathogens influence innate immunity are largely conserved, therefore we believe that our studies pave the way to develop strategies aiming to improve the outcome of microbial infections. 1

U.S. National Science Foundation

NSF is committed to securing the nation's research enterprise as part of its core mission. The Research on Research Security (RoRS) program will advance the understanding of the full scope, potential, challenges, and nature of the research on research security field through scholarly evidence. Background The following activities provide background and context for developing proposals to submit to the RoRS program. The foundational legislative and policy documents include National Security Presidential Memorandum-33 (NSPM-33)and its associated supporting documents, as well as research security provisions in CHIPS and Science Act 2022. In 2022 NSF asked JASON to consider what a research program on research security might entail and how it would be defined.The findings are summarized in the report (JSR-22-08), Research Program on Research Security. The 2024 NSF-funded workshop, Responsible Collaboration Through Appropriate Research Security: A Workshop To Discuss and Study the Emergent Discipline of Research on Research Security, identified current themes, major issues, and challenges in research security. Program Description Collectively, the research that RoRS funds will foster a broad community that builds collaborations between the STEM research community, research security researchers, and research security practitioners. Interdisciplinary approaches are encouraged, and proposers should address how they will leverage the range of expertise, theories, and methods of the team to engage in evidence-based research on research security. Proposers are encouraged to identify collaborators across a wide range of sectors, and to consider projects in collaboration with international partners that share U.S. concerns with research security, when appropriate. RoRS encourages the following types of proposals to help build the emerging field of research on research security. (See the PAPPG for guidance on preparing specific proposal types.) Conferences and Workshops Planning Grants Early-concept Grants for Exploratory Research (EAGER) Proposal topics may include, but are not limited to, the following: The nature and pervasiveness of research security threats. Methods for identifying research security risks, and strategies for preventing and mitigating them. Methods for strengthening research security protocol and approaches. The complex relationships between human behavior and research security policies. Research security policies and their implications. Research on organizational change around systemic and cultural factors as they pertain to research security. Research on research security in the context of a particular field or discipline, especially in high-risk areas. The international dimensions of research security. Collectively, RoRS seeks to fund research projects with the following characteristics: Produce data, analysis, theory, and tools that inform current and future decision-making on U.S. research security. Use rigorous empirical methods to advance understanding of the factors that influence research security. Build upon established methodologies from diverse fields of study to ensure that RoRS develops quickly and efficiently into a robust, mature discipline with its own novel approaches. Develop innovative strategies to leverage previously unidentified, unconnected, and/or inaccessible sources of data. Prospective PIs are strongly encouraged review NSF Research Security resources and to contact the cognizant RoRS program director(s) prior to submission. Proposals should be prepared and submitted following the guidance in the NSF Proposal & Award Policies & Procedures Guide (PAPPG).

U.S. National Science Foundation

NSF is committed to securing the nation's research enterprise as part of its core mission. The Research on Research Security (RoRS) program will advance the understanding of the full scope, potential, challenges, and nature of the research on research security field through scholarly evidence. Background The following activities provide background and context for developing proposals to submit to the RoRS program. <ul> <li>The foundational legislative and policy documents include <a href="https://trumpwhitehouse.archives.gov/presidential-actions/presidential-memorandum-united-states-government-supported-research-development-national-security-policy/">National Security Presidential Memorandum-33 (NSPM-33)</a>and its associated supporting documents, as well as research security provisions in CHIPS and Science Act 2022.</li> <li>In 2022 NSF asked JASON to consider what a research program on research security might entail and how it would be defined.The findings are summarized in the report (JSR-22-08), <a href="https://nsf-gov-resources.nsf.gov/2023-03/JSR-22-08%20NSF%20Research%20Program%20on%20Research%20Security_03152023_FINAL_1.pdf?VersionId=lwtxqUjbqGNmbtJ7E66IqQBbt9gzCV8A">Research Program on Research Security</a>.</li> <li>The 2024 NSF-funded workshop, <a href="https://www.nsf.gov/cgi-bin/good-bye?https://www.bakerinstitute.org/research/responsible-collaboration-through-appropriate-research-security">Responsible Collaboration Through Appropriate Research Security</a>: A Workshop To Discuss and Study the Emergent Discipline of Research on Research Security, identified current themes, major issues, and challenges in research security.</li> </ul> Program Description Collectively, the research that RoRS funds will foster a broad community that builds collaborations between the STEM research community, research security researchers, and research security practitioners. Interdisciplinary approaches are encouraged, and proposers should address how they will leverage the range of expertise, theories, and methods of the team to engage in evidence-based research on research security. Proposers are encouraged to identify collaborators across a wide range of sectors, and to consider projects in collaboration with international partners that share U.S. concerns with research security, when appropriate. RoRS encourages the following types of proposals to help build the emerging field of research on research security. (See the <a href="https://www.nsf.gov/policies/pappg">PAPPG</a> for guidance on preparing specific proposal types.) <ul> <li>Conferences and Workshops</li> <li>Planning Grants</li> <li>Early-concept Grants for Exploratory Research (EAGER)</li> </ul> Proposal topics may include, but are not limited to, the following: <ul> <li>The nature and pervasiveness of research security threats.</li> <li>Methods for identifying research security risks, and strategies for preventing and mitigating them.</li> <li>Methods for strengthening research security protocol and approaches.</li> <li>The complex relationships between human behavior and research security policies.</li> <li>Research security policies and their implications.</li> <li>Research on organizational change around systemic and cultural factors as they pertain to research security.</li> <li>Research on research security in the context of a particular field or discipline, especially in high-risk areas.</li> <li>The international dimensions of research security.</li> </ul> Collectively, RoRS seeks to fund research projects with the following characteristics: <ol> <li>Produce data, analysis, theory, and tools that inform current and future decision-making on U.S. research security.</li> <li>Use rigorous empirical methods to advance understanding of the factors that influence research security.</li> <li>Build upon established methodologies from diverse fields of study to ensure that RoRS develops quickly and efficiently into a robust, mature discipline with its own novel approaches.</li> <li>Develop innovative strategies to leverage previously unidentified, unconnected, and/or inaccessible sources of data.</li> </ol> Prospective PIs are strongly encouraged review <a href="https://new.nsf.gov/research-security">NSF Research Security</a> resources and to contact the cognizant RoRS program director(s) prior to submission. Proposals should be prepared and submitted following the guidance in the <a href="https://new.nsf.gov/policies/pappg">NSF Proposal &amp; Award Policies &amp; Procedures Guide (PAPPG)</a>.

NICHD - Eunice Kennedy Shriver National Institute of Child Health and Human Development

PROJECT ABSTRACT The development of the human placenta depends on proper differentiation of the epithelial trophoblasts. Defects in trophoblast differentiation, particularly toward the extravillous trophoblast (EVT) lineage, are associated with adverse pregnancy outcomes. However, the mechanisms that regulate the differentiation of the germinative cytotrophoblasts to EVTs remain unknown. The imprinting disorder Beckwith-Wiedemann Syndrome (BWS) is characterized by abnormal EVT morphology and can offer insights into candidate regulators of EVT differentiation. BWS is most often caused by dysregulation of a cluster of imprinted genes whose expression from the maternal allele is controlled by the imprinting control region IC2. In the human placenta, the IC2- regulated genes are CDKN1C, PHLDA2, SLC22A18, and KCNQ1. Both CDKN1C and PHLDA2 are upregulated over the course of EVT differentiation, are associated with placental phenotypes in knockout mice, and have been previously shown to influence the activity of the transcription factor ASCL2, a critical regulator of EVT differentiation. Therefore, CDKN1C and PHLDA2 most likely drive the EVT phenotypes in BWS. However, the mechanisms underlying the role of the IC2 genes in EVT differentiation and the interactions between these genes remain unexplored. In Aim 1, I will establish the role of the IC2 genes in EVT differentiation. I hypothesize that CDKN1C and PHLDA2 act synergistically to promote EVT differentiation by altering the activity of the transcription factor ASCL2. I will investigate this hypothesis by knockdown of the IC2 genes in human trophoblast stem cells, which can be differentiated into EVTs in vitro, and by characterizing EVTs in BWS patient placentas. Aside from their role in EVT differentiation, the factors that regulate the expression of CDKN1C and PHLDA2 in this process are unknown. Both genes are upregulated in EVT differentiation without changes in methylation at their promoters or the imprinting control region IC2. This implies that there are uncharacterized enhancers regulating the expression of CDKN1C and PHLDA2. For many imprinted genes, promoter-enhancers interactions are mediated by CTCF-dependent contacts with their imprinting control region; however, the CTCF landscape of the IC2 region during EVT differentiation has not been explored. In Aim 2, I will establish the mechanism regulating CDKN1C and PHLDA2 expression in EVT differentiation. I hypothesize that CDKN1C and PHLDA2 are regulated in EVT differentiation by uncharacterized enhancers and that contact with these enhancers depends on contact with IC2 through CTCF-mediated chromatin looping. To test this hypothesis, I will investigate the impact of maternal IC2 deletion and CTCF depletion on IC2 gene expression and EVT differentiation efficiency in iPSC-derived human trophoblast stem-like cells. I aim to establish the role and regulation of the IC2 imprinted cluster in EVT differentiation. By identifying novel regulators of EVT differentiation, I will improve our understanding of this fundamental process in placental development.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

Abstract Myelodysplastic syndromes (MDS) are a group of diverse malignant hematological disorders that originate from hematopoietic stem cells (HSCs). Increased levels of reactive oxygen species (ROS) and DNA damage are commonly detected in hematopoietic cells from MDS patients. An elevated level of ROS, generated from either endogenous or exogenous sources including oncogene activation, leads to loss of quiescence and self-renewal of HSCs. ROS-induced DNA damage speeds up the aging process of stem cells and contributes to the mutagenesis associated with cancer development. m6A RNA methylation plays a significant role in multiple biological processes by introducing another layer of post-transcriptional regulation of gene expression within cells. The goal of this project is to elucidate the significant role of ALKBH5-mediated epigenetic regulation in the maintenance of genomic stability in hematopoietic stem/progenitor cell (HSPCs) during oxidative stress, and how deregulation of ALKBH5 contributes to promotion of leukemic transformation of HSPCs in the initiation and development of MDS. We found that ROS significantly increased global m6A RNA methylation in human cell lines, and that the elevation of m6A mRNA methylation is required for rapidly repairing ROS-induced DNA lesions and preventing cell death. Interestingly, we found that ALKBH5, the m6A RNA demethylase, is responsible for ROS-induced elevation of m6A mRNA methylation. ROS induced post- translational modification of ALKBH5, and inhibited the demethylase activity of ALKBH5. We showed that forced expression of ALKBH5 inhibited ROS-induced m6A mRNA methylation and significantly delayed repair of ROS-induced DNA damage. Thus, we hypothesize that aberrant expression of ALKBH5 disrupts HSPC functions by negatively influencing genome integrity and survival of HSPCs, thereby contributing to leukemic transformation of HSPCs during the initiation and development of MDS. In this proposal, we will determine 1) the role and underlying mechanism of ALKBH5 in the maintenance of genomic stability in HSPCs in response to oxidative stress; 2) the effects of ALKBH5/Alkbh5 overexpression on the maintenance of mouse and human primary HSPCs during ROS stress in vivo; and 3) whether ALKBH5/Alkbh5 is required for the maintenance of pre-leukemic stem cells (pre-LSCs) in MDS. Our study will provide new insights into novel mechanisms of MDS development and epitranscriptional regulation of gene expression in HSPCs in response to oxidative stress. Additionally, our study will provide the first set of evidence to support a significant role of ALKBH5- mediated m6A mRNA demethylation in the maintenance of normal HSPCs and pre-leukemic stem cell (pre- LSCs).

NCI - National Cancer Institute

Breast tissue is dynamic and undergoes significant structural changes throughout a woman's life. The breast tissue architecture is maintained by a population of stem cells with self-renewal capacity which are essential for tissue repair and remodeling. Recently, the role of stem cells in breast carcinogenesis has been recognized as a high priority for translational breast cancer (BCa) research. The stem cell hypothesis of breast carcinogenesis suggests that breast cancer development might be directly related to the size of the stem cell pool and its mitotic activity. Further, in the mammary gland, stem cells are the only cell subpopulation that has capacity to accumulate all the oncogenic alterations. This project will fill gaps in our understanding of the role of stem cells in the early stages of breast carcinogenesis and their interplay with BCa risk factors by focusing on co-stained stem cell marker combinations that are reflective of high-risk stem cell lineages. Specifically, we will explore: 1) the associations of high-risk stem cell lineages (CD44+/CD24-/low, EpCAM-/low/CD49fhigh and ALDH1A1high/CD44+/CD133+) in histologically normal breast tissue with mammographic percent density and AI- based mammographic features (n=1,290); 2) the associations of high-risk stem cell lineages with subsequent BCa risk in women with a previous benign biopsy (444 cases/1,003 controls); and 3) the associations of hormone-related factors (oral contraceptives, menopausal hormone therapy, alcohol use, body mass index, weight gain since age 18, and reproductive factors) with high-risk stem cell lineages (n=1,834). We will use prospectively collected data/samples/ mammograms from cancer-free women with benign breast disease (BBD) within the Nurses' Health Study (NHS), NHS II, Washington University's Women's Health Repository (WHR), and a unique collection of data/samples/mammograms from healthy women in the Komen Tissue Bank, with the final study population representative of US demographics. Stem cell markers will be stained on study tissue microarrays (specifically constructed from histologically normal breast tissue regions) with commercially available antibodies using multiplex immunofluorescence, and the staining results will be evaluated with automated image analysis. We propose a highly novel investigation that will comprehensively examine the role of stem cell markers in breast carcinogenesis. The study aims to shed light on molecular pathways behind the observed associations of risk factors with BCa risk as well as to identify markers that could advance future risk prediction in a large segment of high-risk women undergoing routine breast biopsies and those with high-risk mammographic features. This proposal could pave the way for novel personalized breast cancer prevention and surveillance strategies. As stem cell activity is potentially modifiable via a variety of targeted therapies, the findings could translate into stem cell -directed pharmaceutical interventions aimed at BCa risk reduction in high-risk women with BBD and/or high mammographic breast density in whom novel prevention strategies are urgently needed.

NINDS - National Institute of Neurological Disorders and Stroke

ABSTRACT The motor symptoms associated with Parkinson’s Disease (PD) are caused by progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). Currently, there is no explanation for what causes this selective cell vulnerability. In addition to age, environmental factors (e.g. exposure to neurotoxins) also increase the risk for PD, but the mechanisms contributing to vulnerability are poorly understood. Further, there are no available treatment options that effectively prevent or slow DA neuron loss or the progression of related symptoms. Thus, there is a significant need for molecular dissection of the key pathways involved in regulating susceptibility to degeneration in order to identify novel potential drug targets and develop improved treatment options for PD patients. Myocyte enhancer factor 2A (MEF2A) was identified as a genetic master regulator whose activity is decreased in the DA neurons of MPTP treated mice. Dysregulation of MEF2A activity is thought to underlie DA neuron vulnerability. Inactivation of MEF2A can occur through phosphorylation of serine 408 (S408) in the carboxy terminal of the protein. The kinases involved in this phosphorylation are known to be activated by environmental exposure to neurotoxins which disrupt mitochondrial function and energy production. My preliminary data in stem cell-derived midbrain DA neurons indicates that in the absence of MEF2A, these cells experience significant changes in the expression of genes associated with synaptic signaling, maintenance of membrane potential, regulation of cell cycle processes, and DNA metabolic processes. My central hypothesis is that MEF2A is a critical regulator of vulnerability because it regulates the expression of other genes necessary for proper DA neuronal function, and that dysregulation of MEF2A activity underlies the DA neuron vulnerability associated with PD pathogenesis. To test this hypothesis, I will carry out two Aims. In Aim 1, I will determine how MEF2A affects intrinsic DA neuron vulnerability. Using in vitro human embryonic stem cell (hESC)-derived midbrain DA neurons, I have generated an inducible MEF2A knockout cell line. I will use this line, along with wild type (WT) DA neurons, to define the role of MEF2A in cell vulnerability using cell death assays, immunohistochemistry, senescence assays, patch clamp electrophysiology, live Ca2+ imaging, and fluorescent mitochondrial ROS assays. In Aim 2, I will look at how environmental factors contribute to MEF2A activity dysregulation and SNpc DA neuron vulnerability. For this, I will use in vitro neurotoxin and kinase inhibitor treatments along with cell death assays and quantitative western blotting to look at changes in survival as well as levels of phosphorylated MEF2A (p-MEF2A) in both WT and MEF2A-KO DA neurons. This proposed research will provide crucial insights into the molecular and cellular mechanism underlying SNpc DA neuron vulnerability and inform future avenues of investigation for the development of preventative treatments for PD patients.

NHLBI - National Heart Lung and Blood Institute

Abstract Hematopoietic stem cell (HSC) transplantation is a potent therapeutic strategy for the treatment of many blood disorders. Therefore, the development of methods for deriving large quantities of HSCs is a major focus in regenerative medicine. Unlike HSCs, human induced pluripotent stem cells (hiPSCs) can be grown indefinitely. Despite hiPSCs being an extremely scalable source, HSCs derived from hiPSCs using current protocols are largely devoid of long-term blood reconstitution potential. These shortcomings are suggestive of knowledge gaps surrounding HSC biology. In the Camargo lab we leveraged our in-vivo barcoding mouse model to show definitively that HSCs arise from both intraembryonic (aorta) and extraembryonic (umbilical and vitelline arteries) sites during native hematopoiesis, and that these sites play differential roles in blood production. Our findings suggest for the first time that umbilical and vitelline (UV) artery HSCs are more short-lived than aortic HSCs, and that the UV artery engages potently in embryonic lymphopoiesis. By performing single cell RNA-seq on murine blood producing endothelial cells, I observed differential NOTCH signaling strength and the presence of NOTCH inhibitors GPR183 and DLK1 in the aorta and UV arteries respectively. While it is vastly appreciated that a transient reduction in NOTCH signaling strength is required for hematopoiesis to occur, no study has detailed differential mechanisms of NOTCH inhibition at spatially distinct HSC-producing sites. Cross-referencing this site-specific data with scRNA-seq on a commonly used hiPSC hematopoietic differentiation protocol, I identified for the first time the exclusive prevalence of the UV-like hemogenic endothelium in vitro. To develop methods of producing long-lived HSCs with adult-like lymphoid potential, we plan to study the Notch pathway as a regulator of site-specific hematopoiesis and modulate NOTCH signaling strength to produce more aortic-like hemogenic endothelium from hiPSCs. From this preliminary data, we hypothesize that differential NOTCH signaling strength is crucial for producing distinct hematopoietic programs in the UV arteries and the aorta. To test this central hypothesis, we plan to pursue the following specific aims: (1) characterize the role of GPR183 in aortic hematopoiesis through murine loss of function studies, (2) describe the role of DLK1 in UV hematopoiesis by murine loss of function, and (3) determine the function of DLK1 in controlling the hiPSC spatial hematopoietic program. From these experiments we expect to elucidate the role of these NOTCH inhibitors in spatially defined hematopoiesis. By leveraging our site-specific scRNA-seq dataset, we are uniquely positioned to produce methods of deriving aortic-like blood cells. These novel blood populations have the potential to revolutionize the therapeutics landscape.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY The intestinal microbiota is a complex community that modulates immune responses and host metabolism. However, colonization of this niche by pathobionts, particularly early in life, can perturb this homeostasis and cause intestinal damage and inflammation. Further, because the neonatal intestinal microbiota, immunity, and barriers are not fully developed, infants are particularly susceptible to pathogen barrier breach and systemic bloodstream infection. Group B Streptococcus (GBS) is one such pathobiont that colonizes the neonatal gastrointestinal tract following aspiration of infected amniotic fluid and/or breast milk. This intestinal colonization serves as a reservoir for “late-onset” GBS systemic disease (LOD), which presents at least one week following birth (typically as bacteremia and/or meningitis) and causes ~15% mortality regardless of antibiotic treatment. Despite this, the mechanisms underlying GBS infant intestinal colonization and resulting systemic neonatal disease remain largely unknown. Type VII secretion systems (T7SS) export effector proteins with functions in virulence, toxicity, or interbacterial killing, and we recently characterized this system in GBS. Our previous work showed that GBS T7SS and its effectors promote virulence in murine models of meningitis by pore-forming effectors as well as female genital tract colonization by toxin-mediated interbacterial competition and immune evasion. We recently found that GBS T7SS is also important for neonatal systemic infection stemming from intestinal colonization and that GBS T7SS effectors are toxic to intestinal epithelium. Based on these data, this proposal will investigate the role of the GBS T7SS in neonatal intestinal dysbiosis, including disruption of the microbiota, impairment of immune responses, barrier breakdown, and ultimately systemic bacterial spread/bacteremia. These questions will be addressed with human cohort data as well as in vitro and in vivo models of GBS intestinal colonization and systemic dissemination in the following aims: AIM 1: Investigate GBS perturbation of the intestinal microbiota during infant intestinal colonization. AIM 2: Evaluate anti-GBS mucosal immune responses during infant intestinal colonization. AIM 3: Determine mechanisms of GBS-mediated inflammation and barrier damage in intestinal epithelium in vitro and during infant intestinal colonization in vivo. This proposal will investigate the role of GBS T7SS effectors on newborn intestinal colonization and barrier loss, which may afford novel targets and alternative therapeutic strategies to treat and prevent neonatal infections.

NCI - National Cancer Institute

PROJECT SUMMARY The main goal of the RUNX1 Research Program 10th Annual Scientific Conference and Patient Meeting is to create a dynamic convening to foster collaboration and provide opportunities for knowledge and data sharing among a diverse set of researchers, clinicians, and patients and their families for a rare disease called RUNX1 familial platelet disorder with predisposition to hematologic malignancies (RUNX1-FPD or FPDMM). Individuals with the disorder have a 35-50% lifetime risk of developing a hematologic malignancy. Of those who develop a malignancy, over 50% are diagnosed with AML. It is the only convening of its kind and continues to be an important part of deepening the communities’ understanding of the disease, of driving collaborations, and facilitating the discovery of future therapies for patients. Equally important is the opportunity for early career investigators, posts, and graduate students to present their research and receive feedback from a diverse, multidisciplinary community, a critical aspect of their training. RRP is committed to cultivating the next generation of RUNX1-FPD basic, translational, and clinical researchers. Conference participation has grown since our first conference in 2017, which had only 18 attendees. By 2021 we had over 181 attendees for the virtual conference. In 2022, we had 130 individuals - 40 patients and 90 scientists, clinicians, and genetic counselors - who attended in person in Princeton, NJ. Thanks to NCATS/NIH funding, we were able to award five (5) deserving young investigators with travel scholarships to attend the conference in 2022 and present at the poster sessions. In 2023, we returned to a virtual format with 397 registrants and a total of 219 participants. Once again, we held a poster session with four (4) young investigators.At our 2024 in-person scientific conference in Princeton, NJ we had 84 scientists, clinicians, and genetic counselors. As a result of NCI funding for the conference, we awarded travel scholarships to six (6) trainees.In 2024, we did not host a formal patient meeting alongside the scientific conference because we decided to pilot a smaller regional patient meeting in Houston to better reach patients outside of the northeast. This decision was influenced by a patient community-wide survey we conducted. Regardless, there were still seven patients and patient family members who attended the scientific conference. In 2025, our scientific conference and patient meeting will be held in September. The agenda includes research-specific sessions open to all stakeholders as well as a track dedicated to RUNX1-FPD patients and family members. The objective is to promote and drive patient-engaged research forward, with direct patient input in the development and planning of the sessions via our 23-member Research Guided by Patients Committee (RGPC). The research-focused portion of the meeting will bring together experts from the fields of hematology, immunology, oncology, cell therapy, and basic science who are committed to uncovering the mechanisms underlying the pathogenesis of RUNX1-FPD with the goal of developing therapeutic interventions that impact the bleeding and immune dysfunction issues and most importantly the predisposition to malignancy. The audience will include investigators devoted to studying RUNX1, leukemia progression, clonal hematopoiesis, gene editing, and hematopoietic stem cell transplants. It has become increasingly clear through the NHGRI-sponsored natural history study of RUNX1-FPD that immune dysfunction and inflammatory disorders are common. RUNX1-FPD includes a unique patient population where there may be a nexus between immunology and oncology based entirely on the reduced and/or altered activity of a single transcription factor, RUNX1.

NIGMS - National Institute of General Medical Sciences

We seek funding to acquire a Thermogravimetric Analyzer (TGA) with Evolved Gas Analysis (EGA) capabilities via selective sampling for GC-MS, to advance materials research and STEM education at the University of North Carolina at Pembroke (UNCP). Currently, UNCP lacks a TGA system, limiting capacity for advanced thermal analysis, reducing research productivity, and requiring reliance on external collaborations that introduce cost and delays. UNCP is a primarily undergraduate institution serving a large student population in a resource-limited region. The proposed instrument will directly support three faculty-led research initiatives—including projects led by early-career investigators—focused on biomass pyrolysis, plastics recycling, and the development of polymeric adsorbents for environmental remediation. The TGA-EGA system will enable precise measurements of decomposition temperatures, small molecule desorption profiles, and trace impurities, which are essential for characterizing complex materials. The instrument will also be integrated into upper-level chemistry courses, including organic, analytical, instrumental, and physical chemistry, providing hands-on training in thermal analysis and macromolecular characterization. These experiences will enhance preparation for careers in STEM and graduate study, strengthening the scientific workforce. The TGA-EGA will be housed in a shared research facility with broad access across departments, supporting interdisciplinary collaboration and student-faculty research. Its acquisition aligns with institutional goals to expand research infrastructure and increase access to advanced instrumentation.

Toyota USA Foundation

Supports innovative STEM education programs that develop students' skills for future careers, with emphasis on project-based learning.