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NIH

We propose to advance a clinical program of neural stem cell therapy for spinal cord injury (SCI) to an IND submission and clinical trial. Our work to date has demonstrated that Neural Progenitor Cells (NPCs) and Neural Stem Cells (NSCs) survive grafting to the spinal cord and extend very large numbers of axons over long distances through the lesioned rodent and large animal spinal cord. Host axons also regenerate into cell grafts occupying the lesion site, and form new synaptic connections that act as neural relays across the injury to support functional improvement in both rodents and large animals. We have identified a lead candidate human NSC/NPC line for clinical translation: an H9 human embryonic stem cell (a federally approved human cell line) that is driven to a spinal cord NSC/NPC fate. We refer to these cells as H9-scNSCs. H9-scNSCs survive grafting to cervical spinal cord hemisection and contusion lesions. This promising line of work is advancing on a translational path, supported extensively by the VA’s RR&D Gordon Mansfield Spinal Cord Injury Consortium. We aim to bring this work to the point of readiness for human clinical trials in SCI. The goal of the current application is to advance this program to submission of an FDA IND, with the eventual goal of a human clinical trial of this promising approach. For the 4 year funding period, this project will support characterization of cells, assay development, IND-enabling in vivo studies, project management and the services of regulatory experts with experience in FDA submissions.

NASA Headquarters

Awards will be made as grants, cooperative agreements, and inter- or intra-agency transfers depending on the nature of the proposing organization and/or project requirements. The period of performance for an award is up to 3 years. Note that it is NASA policy that all investigations involving non-U.S. organizations will be conducted on the basis of no exchange of funds. Prospective proposers are requested to submit any questions in writing to nice-questions@lists.nasa.gov no later than 10 business days before the proposal due date so that NASA will be able to respond. Only Tribal Colleges and Universities that are legally recognized by the Department of Education are eligible to apply for this NASA Research Announcement (NRA). No later than the due date for proposals, proposers to this NRA are required to have: 1) a Data Universal Numbering System (DUNS) number, 2) a valid registration with the System for Award Management (SAM) [formerly known as the Central Contractor Registry (CCR)], 3) a valid Commercial And Government Entity (CAGE) Code, 4) a valid registration with NASA Solicitation and Proposal Integrated Review and Evaluation System (NSPIRES) (this also applies to any entities proposed for subawards or subcontracts.) Consult App F Section F.2.1 and F.2.2 regarding teaming requirements and partnership guidelines. The goals of the NASA Innovations in Climate Education Tribal (NICE-T) activity are to use NASA s unique contributions to climate and Earth system science, through collaboration with tribal institutions, to improve the quality of the Nation s STEM (Science, Technology, Engineering and Mathematics) education to: Increase the level of climate literacy and engagement of the United States public. Create a diverse, highly skilled, and motivated future workforce in climate-related sciences. Advance the understanding of how to effectively teach global climate change concepts. Grantee institutions have the responsibility for budgeting and documenting compliance with Code of Federal Regulations, 14 CFR 1230, commonly referred to as the Common Rule for the Protection of Human Subjects. Research to develop NASA-themed exhibits, programs, curriculum products, etc., may involve full human subjects review through an Institutional Review Board (IRB) or it may be exempt. An IRB also certifies when research is exempt. Every institution that intends to submit a proposal to this NRA, including the proposed prime award or any partner whether an informal education institution, other non-profit institutions, state and local Government agencies, and other organizations that will serve as subawardees or contractors, must be registered in NSPIRES. Electronic submission of proposals is required by the due date and must be submitted by an authorized official of the proposing organization. Such registration must identify the authorized organizational representative(s) who will submit the electronic proposal. All principal investigators and other participants (e.g. co-investigators) must be registered in NSPIRES regardless of submission system. Potential proposers and proposing organizations are urged to access the system(s) well in advance of the proposal due date(s) of interest to familiarize themselves with its structure and enter the requested information. Electronic proposals may be submitted via the NASA proposal data system NSPIRES or via Grants.gov. Organizations that intend to submit proposals via Grants.gov must be registered 1) with Grants.gov and 2) with NSPIRES. Additional programmatic information for this NRA may develop before the proposal due date. If so, such information will be added as a Frequently Asked Question (FAQ) or formal amendment to this NRA and posted on http://nspires.nasaprs.com . It is the proposer s responsibility to regularly check NSPIRES for updates to this NRA. When the NICE-T portal page on NSPIRES is updated a notice will be added to the NASA Education Express weekly news service. To subscribe to NASA Express, go to http://www.nasa.gov/education/express .

NASA Headquarters

Awards will be made as grants, cooperative agreements, and inter- or intra-agency transfers depending on the nature of the proposing organization and/or project requirements. The period of performance for an award is up to 3 years. Note that it is NASA policy that all investigations involving non-U.S. organizations will be conducted on the basis of no exchange of funds. Prospective proposers are requested to submit any questions in writing to tcu-elo-questions@lists.nasa.gov no later than 10 business days before the proposal due date so that NASA will be able to respond. Only Tribal Colleges and Universities that are legally recognized by the Department of Education are eligible to apply for this NASA Research Announcement (NRA). No later than the due date for proposals, proposers to this NRA are required to have: 1) a Data Universal Numbering System (DUNS) number, 2) a valid registration with the System for Award Management (SAM) [formerly known as the Central Contractor Registry (CCR)], 3) a valid Commercial And Government Entity (CAGE) Code, 4) a valid registration with NASA Solicitation and Proposal Integrated Review and Evaluation System (NSPIRES) (this also applies to any entities proposed for subawards or subcontracts.) Consult Appendix E Section E.2.1 and E.2.2 regarding teaming requirements and partnership guidelines. The goals of the TCU ELO are to utilize NASA s unique contributions in collaboration with tribal colleges and universities and tribal-serving institutions to improve the overall quality of the Nation s STEM (Science, Technology, Engineering and Mathematics) education. To achieve these goals, NASA TCU ELO seeks to: Increase learners' involvement and interest in STEM, educate them on the value of STEM in their lives, and positively influence the perception of their ability to participate in STEM; Strengthen efforts to attract and retain increased numbers of students in NASA STEM programs to encourage their pursuit of educational disciplines and careers critical to NASA s and the Nation s future engineering, scientific, and technical workforce; Provide opportunities for TCU students, faculty and staff; and high school students who are likely to matriculate to TCUs, to engage in NASA-related STEM scientific research and engineering activities; Expand outreach activities between NASA and tribal colleges and universities to increase TCU access to NASA s unique science and exploration assets and data in the creation of experiential learning opportunities for students; Enhance NASA s knowledge of the unique TCU assets and requirements, and enhance NASA-TCU partnerships Grantee institutions have the responsibility for budgeting and documenting compliance with Code of Federal Regulations, 14 CFR 1230, commonly referred to as the Common Rule for the Protection of Human Subjects. Research to develop NASA-themed exhibits, programs, curriculum products, etc., may involve full human subjects review through an Institutional Review Board (IRB) or it may be exempt. An IRB also certifies when research is exempt. Explanation of Other Category of Funding Activity TCU-ELO may be categorized as both Science and Technology and other Research and Development (ST) and Education funded activity. Every institution that intends to submit a proposal to this NRA, including the proposed prime award or any partner whether an informal education institution, other non-profit institutions, state and local Government agencies, and other organizations that will serve as subawardees or contractors, must be registered in NSPIRES. Electronic submission of proposals is required by the due date and must be submitted by an authorized official of the proposing organization. Such registration must identify the authorized organizational representative(s) who will submit the electronic proposal. All principal investigators and other participants (e.g. co-investigators) must be registered in NSPIRES regardless of submission system. Potential proposers and proposing organizations are urged to access the system(s) well in advance of the proposal due date(s) of interest to familiarize themselves with its structure and enter the requested information. Electronic proposals may be submitted via the NASA proposal data system NSPIRES or via Grants.gov. Organizations that intend to submit proposals via Grants.gov must be registered 1) with Grants.gov and 2) with NSPIRES. Additional programmatic information for this NRA may develop before the proposal due date. If so, such information will be added as a Frequently Asked Question (FAQ) or formal amendment to this NRA and posted on http://nspires.nasaprs.com . It is the proposer s responsibility to regularly check NSPIRES for updates to this NRA.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY 2025 Rachmiel Levine-Arthur Riggs Diabetes Research Symposium November 14-17, 2025, Westin Pasadena, Pasadena, CA Despite the significant knowledge obtained and the progress made in the treatment of diabetes over the last 50 years since the discovery of insulin, translation of this understanding to the clinic, and implementation of acceptable standards of care for diabetics has been suboptimal. In view of the rapidly growing worldwide diabetes epidemic - the disease affected 22.3 million people in the USA and 371 million people worldwide in 2012, and is expected to double by 2030 if current trends hold - it is imperative to enhance current interactions among investigators. This is to foster new collaborations, and pool knowledge and resources so that the cellular and molecular mechanisms responsible for the disease and its complications can be determined, and novel therapeutic strategies developed that will effectively prevent, delay, and even cure diabetes. The 2025 Rachmiel Levine-Arthur Riggs Diabetes Research Symposium, to be held from November 14-17, 2025 at The Westin in Pasadena, California, will continue to meet the growing demand to keep researchers, clinicians and trainees abreast of the latest developments in diabetes- and endocrine-related research. The Symposium is organized by the City of Hope’s Arthur Riggs Diabetes and Metabolism Research Institute (AR-DMRI) and is expected to attract over 250 attendees from both the U.S. and abroad with diverse academic backgrounds including, endocrinologists, diabetologists, islet biologists, stem cell and gene transfer scientists, transplant scientists, immunologists, cell biologists, young investigators in all these areas, and health care professionals who manage individuals with diabetes. The four-day meeting will offer presentations from over 60 experts in the field of type 1 diabetes and islet cell biology. The meeting will consist of introductory lectures and plenary sessions that will each conclude with a panel discussion. In addition, the meeting will offer a debate session, oral presentations from junior investigators and trainees, and a poster session for both junior and established investigators to present new and exciting data. The Symposium provides an important venue for investigators to present their data to an audience of national and international experts, helping to foster the career growth of junior investigators.

NIDCR - National Institute of Dental and Craniofacial Research

Project Summary Craniofacial differences are among the most common congenital anomalies, occurring with a frequency of 1 in 700 live births. The biomedical burden for treating these conditions is over 700 million dollars a year in the US alone. Thus, assembling a group of discovery-based research scientists, geneticists, clinicians, and surgeons all focused on understanding the genetic, molecular, and cellular mechanisms essential for understanding craniofacial development and disease is of great value to public health. To address this need we have formulated a scientific program that will focus on integrating our knowledge of genetics, model systems, and biological mechanisms, with the end goal of improving craniofacial health. A keynote session will explore rare disease genetics from both a human geneticist and research perspective. Challenges and solutions related to linking gene discovery to functional genomics will be identified, with a focus on advancing the craniofacial field into the era of stem cell and organoid medicine. Molecular and biochemical mechanisms that contribute to patterning the building blocks of the face will be discussed, alongside how these mechanisms go awry under pathological conditions. Cross-disciplinary collaboration will be promoted to ensure translationally relevant data is shared, facilitating the realization of the bench-to-bedside vision from diagnosis to therapeutics. Open discussion within the community will aim to establish a consistent set of protocols for data comparison and reproducibility across laboratories, enhancing the efficiency and impact of craniofacial research. Beyond sharing cutting-edge, unpublished research, the meeting will provide opportunities for scientists at all career levels to network and form collaborations with colleagues from various disciplines to advance craniofacial research.

NIAMS - National Institute of Arthritis and Musculoskeletal and Skin Diseases

PROJECT SUMMARY Adult epithelia regenerate during adult life due to the constant activity of stem cell pools. Stem cells maintain tissue homeostasis and repair injury by close communication with their tissue environment, known as "niche.” Niches are complex, structured arrays of different cell types that guide tissue stem cell dynamics. The ultimate goal of understanding epithelial stem cell regulation is to repair or replace cells or organs damaged by injury, disease, and aging. The strategies vary from generating cell types and tissues in a dish for transplantation purposes to directly stimulating the damaged organ in the living organism. This field has been exponentially growing for the past decade. Tissues such as human skin and cornea have already been grown in 3D cultures and used in clinics to fight otherwise incurable medical conditions. The GRC on Epithelial Stem Cells and Niches will focus on comparative principles of adult epithelial stem cell dynamics and niche signaling across tissues. This conference will include work on the molecular control of stem cell function from the epidermis and its appendages, intestine, lung, mammary gland, cornea, prostate, and emerging work from other epithelial tissues. Research from all model organisms will be represented, fostering a comprehensive discussion on epithelial stem cell biology. Following its inaugural meeting in 2016, this GRC has held successful meetings in 2018, 2022, and 2024. In the 2026 meeting we will continue to bring in both new and veteran speakers to allow a variety of participants to contribute to this exciting event over the coming years. In particular, for the 2026 meeting, we have built a scientific program that emphasizes key cutting-edge areas in epithelial biology, including interorgan communication, microbe-immune-epithelial interactions, stemness and plasticity, and epithelial aging. These themes reflect the fields shift toward understanding organs as interconnected systems and addressing the challenges of tissue dysfunction in aging and disease. In addition, we will support the attendance of graduate students, postdocs, and early career scientists as they make their way into this exciting field of study by hosting a GRS in the two days prior to this GRC. A critical feature of the GRC’s scientific mission is to engage the next generation of scientists. We are continuing our two-day Gordon Research Seminar (GRS) for graduate students and postdoctoral fellows that will precede this GRC. The GRS will allow students and fellows to share and discuss unpublished data and technical breakthroughs, favoring collaborative efforts and sparking provocative hypotheses to be discussed on the floor of the main conference. Furthermore, the participants will have the opportunity to establish tight professional relationships from which they will benefit throughout their careers. GRS participants will be expected to stay for the GRC, further contributing to the educational value of this conference.

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

Project Summary Autism Spectrum Disorder (ASD) affects roughly 1% of the world’s population, and currently, there are no mechanism-based treatments that address the core features of ASD. It is now clear that the genetics underlying ASD are complex; with several hundreds of genes conferring large risk as well as common variants contributing to a large proportion of ASD heritability. Genetic studies of ASD suggest a high degree of convergence on specific cellular processes and biochemical pathways, which have led researchers to posit that potential therapeutic strategies may be shared across different genetic etiologies. The study of monogenic or syndromic forms of ASD has been a leading strategy to gain insight into the complex mechanisms of ASD. Fragile X Syndrome (FXS) is among the leading monogenic causes of ASD and is the most common inherited cause of intellectual disability. Since the Fragile X gene (FMR1) was cloned in 1991, the field has used cellular assays and model organisms to elucidate the functions of the FMR1 protein (FMRP), the consequences of its loss, and identify therapeutic targets for FXS and ASD. Other “syndromic” forms of ASD, such as tuberous sclerosis complex, Rett Syndrome, Angelman Syndrome, CHD8, NRXN1 and others, are being investigated using similar approaches. Recent technological advances in stem-cell derived neurons, single cell sequencing, gene therapy, human neurons, and organoids are setting the stage for transformative advances in therapeutic development for these neurodevelopmental disorders. This conference will bring together leading basic and translational scientists studying ASD, Fragile X and related neurodevelopmental disorders from around the world with the ultimate goal of developing mechanism-based treatments that address the core features of these diseases.

NCI - National Cancer Institute

PROJECT SUMMARY/ABSTRACT This conference grant application requests funds to help support the Gordon Research Conference (GRC) on Nasopharyngeal carcinoma (NPC) May 10 - 15, 2026. NPC is a deadly cancer arising in the nasopharynx which has high incidence in particular regions, including Alaska. The peak age at NPC diagnosis is in the mid-forties, which is two decades earlier than for many other common cancers. Thus, NPC has a significant socioeconomic impact globally. The etiology of this unique cancer includes three significant co-factors: host genetics, Epstein- Barr Virus (EBV) infection, and environmental influences. How these factors contribute to NPC development is the research focus of numerous labs worldwide. Because of its proclivity for early lymphatic spread, NPC is often diagnosed at an advanced stage, when the cancer is harder to cure and requires aggressive treatment. An enhanced understanding in regard to how EBV and aberrations in cell signaling drive normal cells to become cancerous, how these cells escape from the immune surveillance, and their molecular signatures for early diagnosis as well as for development of novel targeted and immune therapy is expected to improve NPC treatment and outcomes. The fact that the development of NPC requires the convergence of many different factors, including Epstein-Barr infection, host genetics, impaired anti-tumor host immune function, and epidemiological factors, makes this unique cancer a powerful model to dissect out the host-virus-environment interactions, thereby yielding insights into tumor pathogenesis. Studying NPC provides opportunities to address contemporary issues in cancer research (for example, tumor microenvironment, tumor immune surveillance, stem cells, epigenetics, cancer vaccine and immunotherapy). We hypothesize that the 2026 meeting, by featuring cutting-edge NPC basic, translational and clinical research, will provide a unique forum for idea exchange among scientists, clinicians, and industry representatives to catalyze the translation of recent advances into patient care. We will address this hypothesis via three specific aims: 1) To advance knowledge of key NPC basic pathogenetic mechanisms and translational research. 2) To highlight recent advances in nasopharyngeal carcinoma diagnosis and treatment. 3) To provide a stimulating forum that strengthens interactions between basic scientists, translational researchers and physicians and also between junior and senior members of the NPC field. We believe that the scientific environment created at the 2026 NPC Gordon Research Conference meeting will help to advance NPC research and to improve NPC patient care.

NHLBI - National Heart Lung and Blood Institute

The 2026 Gordon Research Conference (GRC) on Plasminogen Activation and Extracellular Proteolysis and the associated Gordon Graduate Research Seminar (GRS) are paired conferences held sequentially at the same location in Ventura, CA. The GRS will take place on February 7-8, and the GRC on February 8-13, 2026. The GRC has been held continuously every two years since 1990 and enjoys an outstanding international reputation. In this 20th GRC, we will discuss breakthrough findings in plasminogen activation and extracellular proteolysis in areas such as vascular biology, central nervous system function and dysfunction, trauma, tissue homeostasis and regeneration, hematopoiesis, angiogenesis, stem cell biology, metabolism and obesity, tumor biology, cardiovascular function, and aging. For the 2026 GRC meeting, emphasis will be placed on bringing together the biomedical practice with the biology of plasminogen activation and other extracellular proteases, their effectors and associated pathways, as they are relevant to multiple diseases and disorders. Basic and Physician Scientists will discuss the relevant clinical needs and possible therapeutic strategies that can be accommodated using the knowledge generated through basic science. Early and mid-career investigators in the field will have the chance to present and discuss their new and exciting findings alongside senior, established researchers. Basic research, technological advances, and cutting-edge therapeutic approaches in the field of extracellular proteases will be debated and discussed, with the expectation that new collaborations and scientific discoveries will develop from these in-person interactions. Research themes of the 2026 GRC on Plasminogen Activation and Extracellular Proteolysis will capture the most exciting areas of contemporary cutting-edge research in the field. Emerging roles for molecules of the fibrinolytic system and other proteases in pathologic settings such as cancer, cardio- and cerebrovascular disease, metabolic complications, aging, trauma, and neurological diseases will be presented. The development and application of novel technologies in the field will also be discussed. Each session will include a discussion of how basic research in our field can help conquer human disease. The associated GRS will provide a venue for pre- and postdoctoral trainees to discuss their research in a collaborative and stimulating environment to help build their informal network of peers and colleagues. We expect that the 2026 Plasminogen Activation and Extracellular Proteolysis GRC and GRS will bring together a group of highly motivated and interactive participants with different scientific backgrounds to engage in intensive discussions at the frontier of research related to the plasminogen activation system and associated extracellular proteases in an “off-the-record” fashion. The information gained from this meeting will advance the plasminogen activation/extracellular proteolysis field by teaching us about additional direct and nuanced roles for these proteins, which should in turn stimulate the development of new applications and strategies to improve the diagnosis, prevention, and treatment of a wide range of diseases.

NEI - National Eye Institute

PROJECT SUMMARY The 2026 Gordon Research Conference (GRC) and Gordon Research Seminar (GRS) on Visual System Development are a paired set of biennial meetings that bring together investigators studying development, disease, and evolution of the visual system. Over the years, these meetings have provided an exciting and unique forum in which to explore the similarities and differences underlying visual system development and function across a broad range of species. The goal of these meetings is to foster an appreciation of common principles that mediate the construction and function of the visual system in diverse organisms, and to share the latest exciting new ideas and findings on this topic. By including sessions that highlight emerging topics with translational impact, such as “Retinal Stem Cells, Repair, and Regeneration”, and “Developmental Disorders, Diseases, and Aging of the Visual System”, the meeting is also expanding its scope and stimulating crosstalk between developmental biologists and investigators focused on translational aspects of vision science. The GRS provides a unique platform for students and postdoctoral research fellows in the visual research field to share current, unpublished research amongst their peers and receive career mentorship in the vision science field. The format of the GRC and GRS meetings provides a highly interactive and stimulating venue for cross- fertilization of ideas and development of new collaborations. The Visual System Development GRC has established a reputation as the leading conference in its field, and it is the only meeting on the topic that brings together vision researchers working on the full range of experimental systems in the field, ranging from Drosophila to human. The current proposal requests funds to help defray conference fees for attendees at both meetings. The Visual System GRC and GRS will feature scientists at the cutting edge of the field, with careful attention taken to ensure involvement of researchers around the world, with participation from scientists at all stages of their careers.

NCI - National Cancer Institute

Chondrosarcoma (CHS), the second most common bone sarcoma, resists chemotherapy, immunotherapy, and radiotherapy and tends to metastasize, posing clinical challenges. In the CHS tumor microenvironment, mesenchymal stem cells (MSCs) and tumor cells act as localized signaling hubs, engaging in continuous bidirectional communication through spatially organized gradients of cytokines and chemokines. These interactions likely induce MSC phenotypic changes that promote tumor growth and metastasis, though the exact mechanisms remain unclear. Current in vitro models fail to replicate these complex interactions, as conditioned medium transfer disrupts continuous signaling, and conventional 3D hydrogel co-culture systems allow paracrine factors to homogenize, erasing essential spatial gradients. To address this gap, we developed EXPECT (EXtrusion Patterned Embedded ConstruCTs), a temperature-sensitive hydrogel system that enables long-term, spatially organized cell-cell communication in 3D. EXPECT uses extrusion bioprinting to embed cell-laden channels and leverages mild temperature actuation to control cell migration. Preliminary studies show EXPECT supports migration along defined axes for up to 36 days, preserving paracrine gradients and enabling the study of sustained MSC-CHS interactions. We hypothesize that temperature actuation in EXPECT preserves spatial gradients, enhancing bidirectional communication between MSCs and CHS cells. This will promote CHS growth, MSC chemotaxis, and phenotypic shifts in MSCs toward a CHS-like profile. Aim 1 investigates cellular level bidirectional crosstalk between MSCs and CHS spheroids within EXPECT. We will co-culture spheroids under temperature actuation for 30 days, hypothesizing that sustained crosstalk drives MSC migration, CHS metabolism, matrix remodeling, and gene expression changes. Aim 2 explores molecular pathways affected by MSC-CHS communication using single-cell RNA sequencing. We expect temperature actuation to activate migratory pathways like PI3K/PIP3 in MSCs, leading to gene expression changes tied to cytoskeletal remodeling, paracrine signaling, and ECM modification, promoting a CHS-like MSC phenotype. EXPECT fills a critical gap in CHS research by enabling studies of sustained MSC-CHS interactions that mimic in vivo conditions. This platform may reveal previously unrecognized crosstalk and MSC phenotypic changes that promote tumor progression, providing new therapeutic targets and improving drug testing models.

NIBIB - National Institute of Biomedical Imaging and Bioengineering

PROJECT SUMMARY Biomaterials for tissue engineering must simultaneously provide mechanical support at the tissue level and local biochemical and physical cues at the cellular level to promote functional tissue regeneration. However, these multiscale requirements often conflict with each other. For example, hydrogels designed to mimic cartilage extracellular matrix typically lack sufficient mechanical strength to withstand forces applied in vivo. Solid scaffolds with load-bearing capability are significantly stiffer than native cartilage. Both examples result in unwanted changes in cellular response that leads to the formation of functionally inferior scar-like tissue. These challenges highlight the critical need for biomaterials with properties that can be independently tuned across multiple length scales to direct functional tissue regeneration. To address this need, a versatile 3D printing approach has been developed to independently control biochemical and physical properties within a single biomaterial. Prior work demonstrated that printing inks containing peptide-functionalized polymer conjugates enabled control of bioactive peptide concentration on the surface without altering scaffold modulus or architecture. In addition, printing with different ratios of polymer molecular weight resulted in scaffolds with significantly different mechanical properties without affecting scaffold architecture, surface chemistry, or crystallinity. Relevant to the proposed work, human mesenchymal stromal cells (hMSCs) cultured in high stiffness scaffolds under chondrogenic (cartilage-promoting) conditions differentiated towards unwanted hypertrophic and osteogenic (bone) lineages while low stiffness scaffolds promoted more stable chondrogenesis. These findings underscore how biochemical and mechanical cues can have competing or synergistic effects and must be optimized independently to direct stem cell fate. The proposed project aims to expand and refine this biomaterial platform using hMSC differentiation toward cartilage as a model system. Specifically, a new approach will be developed to functionalize the surface of 3D-printed solid scaffolds with soft, hydrophilic peptide-polymer bottlebrushes to independently control surface and bulk properties across length scales within a single construct. It is hypothesized that the surface-grafted bottlebrushes will create a soft, hydrogel-like microenvironment for cells without compromising bulk scaffold modulus, and that including bioactive cartilage-promoting peptides will synergistically enhance hMSC differentiation into cartilage cells. This hypothesis will be tested through two Specific Aims: (1) demonstrate that surface properties can be tuned independently of bulk scaffold modulus, and (2) demonstrate that surface-grafted peptide-polymer bottlebrushes enhance hMSC differentiation. This work will provide a powerful and adaptable platform for future biomaterial designs by enabling independent control of cell- material interactions at multiple length scales. The proposed strategy can be broadly applied to other tissue applications by varying peptide sequences, bottlebrush compositions, and bulk scaffold materials.

3M Foundation

Funds STEM education, community development, and environmental sustainability in 3M plant communities worldwide.

DEPT OF DEFENSE.DEPT OF THE NAVY.NAVSUP.NAVSUP WEAPON SYSTEMS SUPPORT.NAVSUP WSS MECHANICSBURG.NAVSUP WEAPON SYSTEMS SUPPORT MECH

48--STEM,FLUID VALVE

NINDS - National Institute of Neurological Disorders and Stroke

PROJECT SUMMARY/ABSTRACT Interspecies blastocyst complementation (IBC) holds great potential to open new avenues for neuroscience, offering a unique perspective on brain development and evolution. This technique introduces donor pluripotent stem cells (PSCs) into host blastocysts lacking essential organ development genes, enabling the formation of interspecies chimeras. Such chimeras allow for the development of donor-cell-enriched organs in host organisms, a method previously applied to create various organs but not yet successful for brain tissue. Our preliminary studies have introduced a C-CRISPR-based blastocyst complementation method (CCBC), enabling the generation of rat forebrain tissue in mice for the first time. This allows us to study brain development and function from an evolutionary angle, potentially transforming brain research and providing a foundation for ethical considerations regarding the use of human PSCs in animal brains. Building on this, our proposal aims to dissect the xenogeneic barriers affecting brain development between mice and rats, explore non-cell autonomous mechanisms in rat-mouse forebrain chimeras, and attempt to create forebrain tissues from a wide rodent species, African pygmy mouse, in mice. Our objectives include: 1) Understanding Xenogeneic Barriers: Investigating the decline in rat cell contribution in chimeric mouse forebrains, potentially due to cell competition, proliferation differences, or cell adhesion incompatibility, and exploring strategies to overcome these barriers. 2) Exploring Non-Cell Autonomous Mechanisms: Examining how rat-mouse chimeras adapt brain size and developmental pace to the mouse host, using multi-omics analyses and interspecies mesenchymal blastocyst complementation to uncover the molecular and cellular basis of these effects. 3) Expanding to Wild Rodent Species: Venturing beyond common laboratory models to study the forebrains of wild rodents, such as the African pygmy mouse, to broaden our understanding of brain development. Our proposed study promises to illuminate fundamental aspects of brain organization, functionality, and evolutionary dynamics.

NIAID - National Institute of Allergy and Infectious Diseases

Infants are especially susceptible to intracellular pathogens because their immune system is not fully equipped to fight against these microorganisms. As a result, infant infections are a leading cause of mortality, with >1.5 million children dying of infections before 5 years of age in 2022 alone. The current consensus is that before birth, conventional T cells are skewed in favor of T regulatory or T helper (Th) 2 responses, leaving neonates and infants more vulnerable to pathogens cleared by Th1 immunity. Therefore, Vγ9Vδ2 (or simply Vδ 2) T cells, are particularly important in early life, because they are poised to secrete Th1 cytokines even before birth and acquire potent cytotoxic function shortly after birth. Despite their protective role against pathogens, human Vδ2 cells, which are absent in mice, are not well studied in neonates and infants. Our long-term goal is to elucidate their functional heterogeneity because understanding their features in the first few months of life will allow us to harness their properties to protect infants from infections. This task is challenging for many reasons, including the difficulty in obtaining samples from the infants at highest risk of early infections, such as premature babies. Our recent observations, obtained using spectral flow cytometry (SFC) and single cell RNA-seq, converge to show phenotypic and functional heterogeneity of cord blood (CB) Vδ2 cells, with heightened stemness compared to their adult counterpart and a cluster of PD1-hi cells (absent in adults) that may follow a distinct functional program specific for the early life stage. We posit that differences in Vδ2 cell cluster composition at birth have functional consequences and result in improved or decreased antimicrobial activity depending on the composition. The resulting overarching hypothesis is that human neonatal V δ2 lymphocytes exist in heterogenous functional/differentiation states impacting host immune competence in the critical early life window. As a multidisciplinary team of immunologists and computational biologists, we propose to characterize cord blood Vδ2 cells in existing specimens, including samples of premature babies, using state of the art techniques –Cellular Indexing of Transcriptomes and Epitopes by sequencing (CITE- seq) and SFC- with the following aims. Aim 1. Evaluate the phenotypic and functional heterogeneity of Vδ2 T cells at birth and in early life in relation to age, with a focus on a unique subset of PD1-hi cells present in cord blood. Aim 2: Assess how the composition of Vδ2 T cells at birth impacts function of these cells at the population level, combining CITE-seq analysis with depletion and transduction experiments. The goal of this proposal is to develop a robust molecular and functional map of a critical subset of innate-like T cells, which will provide a valuable reference for the cellular heterogeneity in the neonatal human immune system and a foundation for future proposals aimed at understanding Vδ2 cell biology in early life.

NIA - National Institute on Aging

Summary/Abstract Vascular pathology has been identified as a critical driver of Alzheimer’s disease. This proposal aims to establish a human induced pluripotent stem cell (iPSC)-derived model to study the impact of genetic and environmental factors on the development of Alzheimer’s disease-related vascular pathology. Most Alzheimer’s disease patients have cerebral amyloid angiopathy (CAA), the symptoms of which include build-up of amyloid around vessels, cerebral hemorrhages, microbleeds, and inflammation. Studies in multiple mouse models of Alzheimer’s disease have demonstrated that hemopoietic-derived brain-resident microglia and circulating monocytes and perivascular macrophages can be protective against CAA. The APOE44 genotype is the strongest genetic risk factor for Alzheimer’s disease and CAA. Despite the clear interplay between Alzheimer’s disease, CAA, and APOE genotype, the molecular mechanisms underlying the vascular changes are not fully understood. These observations motivate us to create a model using human cells to study the underlying mechanisms of microglia- vascular interactions in cells of different APOE genotypes. In prior published studies, we created a 3D human iPSC-derived vascular model in a hydrogel scaffold. It undergoes vasculogenic and angiogenic events and forms a model plexus (the VAMP model). We showed that the VAMP model can be built inside a microfluidic device to enable regulatable perfusion, mimicking blood flow. We have advanced the model by incorporating microglia (VAMP-MG) to reflect the key cell-cell interactions in CAA better. The work proposed in two specific aims will increase the utility of the VAMP-MG model in five significant ways: We will 1) build the model from a recently established collection of APOE44 versus APOE33 isogenic iPSC lines to incorporate genetic risk factors; 2) incorporate live reporters to monitor the activation states of microglia and vascular cells in real-time; 3) create the VAMP-MG model in microfluidic chips to achieve perfusable vasculature; 4) flow human plasma from Alzheimer’s disease, aged-matched healthy, or young healthy donors through the vessels to improve modeling of disease-relevant environmental factors; 5) use Ribo-Tag technology to identify transcriptomic changes in the vascular endothelial cells and the microglia. The model will be deeply characterized and validated at cellular and molecular levels. Alzheimer’s disease-relevant phenotypes, including amyloid deposition and clearance, A secretion, and inflammatory factor production, will be assessed. We will compare transcriptomic data collected from the model to published human Alzheimer’s disease brain versus healthy control brain transcriptomic data, including single nuclear RNA-seq datasets. Completing the proposed work will enhance our ability to study vascular and microglial responses to inflammatory signals in real time, generate transcriptomic data at cell type levels, and establish APOE44 versus APOE33 phenotypes in microglia-vascular models to a new level of complexity. In the future, this VAMP-MG model can potentially define key genetic and environmental factors that exacerbate or alleviate Alzheimer’s disease-vascular phenotypes.

NCATS - National Center for Advancing Translational Sciences

Human induced pluripotent stem cells (hiPSCs) are a foundational technology for regenerative medicine, disease modeling, and cell-based therapies. However, the clinical translation of hiPSC-derived therapeutics is constrained by unresolved challenges in manufacturing scalability, product consistency, and long-term storage. Current production methods, such as static culture or stirred-tank bioreactors, either lack throughput or impose damaging shear forces that compromise cell viability and stemness. Additionally, existing cryopreservation strategies are not optimized for the large-volume required for centralized manufacturing and distributed clinical deployment. To address these bottlenecks, we propose to develop a modular, low-shear, perfusion-based biomanufacturing platform coupled with controlled-rate cryopreservation for scalable and reproducible expansion of hiPSCs. This R21 will establish the technical feasibility and foundational workflows for a generalizable manufacturing system suitable for diverse therapeutic applications. In Aim 1, we will engineer and optimize a multilayer, perfusion-based bioreactor system to support hiPSC expansion at clinical scales. We will define operational parameters, evaluate multiple hiPSC lines, and develop protocols for efficient harvesting and redeployment. In Aim 2, we will implement long-term culture strategies to preserve genomic stability and pluripotency across multiple passages and optimize cryopreservation workflows using cryobags and controlled-rate freezing. Post-thaw cells will be assessed for viability, genomic integrity, and differentiation potential. Successful completion of this project will yield the first integrated platform for low-shear, current Good Manufacturing Practice (cGMP)-compatible expansion and cryostorage of hiPSC-derived therapeutic products. This innovation will reduce production variability, enhance scalability, and enable rapid deployment of hiPSC-based therapies across a range of disease indications. The resulting system will serve as a flexible and translational foundation for future commercial partnerships and larger-scale studies, consistent with the high- risk, high-reward goals of the R21 mechanism.

NHLBI - National Heart Lung and Blood Institute

Project Summary/Abstract Cardiac fibrosis compromises left ventricular (LV) function and worsens clinical outcomes in heart failure (HF). Currently, there are no clinical therapies that target fibrosis in the failing heart. Platelet-derived growth factor (PDGF), a central mediator of fibrotic responses, acts via two receptors - PDGFRα and PDGFRβ. Our pilot studies using explant cultures, flow sorting, single cell RNA sequencing (scRNAseq), and in vivo mouse models have uncovered a novel stem cell antigen(Sca)-1-expressing PDGFRα+ multipotent cardiac fibroblast population that sources myofibroblasts, interacts with tissue macrophages, and drives fibrotic and inflammatory responses during adverse LV remodeling. During HF, these cells decrease PDGFRα expression and instead upregulate PDGFRβ. The role of PDGFRβ in cardiac fibroblast biology in HF is unknown. We propose the novel hypothesis that a heretofore unrecognized Sca-1+PDGFRβ expressing cardiac fibroblast with mesenchymal stem cell features (termed cFMSCs) are key drivers of a PDGFRβ-dependent immunofibrotic axis in HF. Three Aims will test this hypothesis. In Aim 1, using a murine coronary ligation model, in vitro studies of cell function, scRNAseq, and inducible cardiac fibroblast-specific and Sca1+ cell-specific PDGFRβ-deletion mouse models, we will comprehensively define the importance of PDGFRβ in cFMSC cell function in ischemic HF. We will isolate Sca1+PDGFRα+ cFMSCs and assess PDGFR β-dependent myofibroblast differentiation, multipotency, downstream signaling and immuno-fibrotic secretome, and cFMSC-macrophage interactions. scRNAseq of sorted cells will assess cFMSC subpopulations and changes in transcriptomic profiles. In Aim 2, we will establish the pathogenetic role of cFMSC-localized PDGFRβ in chronic HF, by using inducible cardiac fibroblast-specific PDGFRβ knockout mice, deleting cFMSC PDGFRβ during chronic HF, and assessing late effects on LV remodeling, fibrosis, tissue macrophages, and inflammatory profiles. To establish necessity of cFMSC PDGFRβ signaling, cardiac fibroblast PDGFRβ loss will be induced by tamoxifen in PDGFRβf/f-Tcf21MerCreMer mice 4 w post- MI and LV remodeling, fibrosis, and tissue macrophage and inflammatory profiles will be assessed 6 w Iater. The effects of sustained cardiac fibroblast PDGFRβ activation on LV remodeling will be assessed using PDGFRβ[S]D849V-Tcf21MerCreMer mice. To establish sufficiency of cFMSC PDGFRβ signaling, we will perform intramyocardial adoptive transfer of sorted PDGFRβ-deficient and -competent Sca1+PDGFRα+ cFMSCs from HF mice into naïve mice and assess late LV remodeling and fibrosis. In Aim 3, we will test potentially translatable therapies to antagonize cFMSC PDGFRβ signaling in chronic HF, including CP-67345, a specific small molecule PDGFRβ inhibitor, fibroblast-targeted nanoparticle delivery of PDGFRβ siRNA, and anti-PDGFRβ neutralizing antibody. We will measure the effects of these therapies on LV remodeling, fibrosis, cFMSC abundance, cardiac macrophages, and tissue inflammation. By conclusively defining the role of cFMSCs and fibroblast PDGFRβ in pathological LV remodeling, these studies will provide novel perspectives on the immunofibrotic response in HF.

NEI - National Eye Institute

Abstract Age-related macular degeneration (AMD) and related macular dystrophies (MDs) are leading causes of adult blindness with limited treatment options. AMD/MDs can present in two forms, geographic atrophy/GA (dry form) and choroidal neovascularization/CNV (wet form). There is strong evidence linking sterile inflammation to AMD/MD pathogenesis and two complement pathway inhibitors are already approved by FDA for treating GA in the dry form of AMD. However, due to limited therapeutic impact and adverse effects of complement inhibitors and other approved drugs for both dry AMD and wet AMD, there is a significant need for novel therapies for AMD/MDs. Our recently published data and preliminary studies identified secretory phospholipase A2-IIA (sPLA2-IIA), a pro-inflammatory enzyme, as a key molecular player in AMD/MD pathogenesis. AMD/MD primarily affect the retinal pigment epithelium (RPE) cells in the eye and patient-derived induced pluripotent stem cell- RPE (iRPE) from AMD and 2 distinct MDs showed elevated levels of sPLA2-IIA. Furthermore, AMD/MD iRPE cultures and AMD donor eyes showed elevated sPLA2-IIA levels in drusen, a pathological hallmark of early AMD/MD that is the key driver of later stage pathologies in AMD/MDs. Notably, pharmacological modulation of sPLA2-IIA activity in AMD and MD iRPE cultures led to reduced drusen. In addition, directly linking elevated sPLA2-IIA activity to AMD/MD pathology, sPLA2-IIA overexpression led to AMD-associated pathological alterations (drusen, Bruch’s membrane thickening, RPE thinning, CNV and visual deficits) in C57BL/6J mice. Altogether, these studies provide a strong rationale for targeting sPLA2-IIA activity in AMD/MDs. Toward this goal, we propose to develop proteolysis-targeting chimeras (PROTAC) compounds for specific inhibition of sPLA2-IIA in AMD/MDs. In initial experiments, we have synthesized a ‘lead‘ PROTAC (UR-00059) that can induce degradation of sPLA2-IIA in iRPE cells with half-maximal degradation concentration DC50 of 295.5 nM. The following milestone-driven aims will allow us to develop an effective PROTAC-based therapy targeting sPLA2-IIA for AMD/MDs. Aim 1: Optimize UR-00059 structure and activity and characterize the target engagement in vivo; Aim 2: Conduct in vivo efficacy studies and non-GLP absorption, distribution, metabolism, and toxicology of UR-00059; Aim 3: Perform IND enabling studies and obtain FDA approval for human testing. Ultimately, the proposed studies will develop a novel PROTAC-based therapy for targeting inflammation, drusen and consequently late stage pathologies of AMD and related MDs.

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

PROJECT SUMMARY Differentiation of human primordial germ cells (hPGCs) from human pluripotent stem cells is the first step toward in vitro gametogenesis, which would enable mechanistic studies and treatment of infertility due to loss of gametes. The mechanisms of hPGC differentiation are poorly understood. As a result, current protocols produce heterogeneous mixtures of hPGC-like cells (hPGCLCs) and other cell types. Our long-term goal is to obtain a systems-level understanding of the signaling and gene regulatory network that control primordial germ cell differentiation in vitro and use this to improve directed differentiation of hPGCLCs for potential therapeutic purposes. The objective of this proposal is to quantitatively determine cell signaling requirements of hPGCLC differentiation with unprecedented spatial and temporal resolution. The central hypothesis is that heterogeneous differentiation and maturation of hPGCLCs is due to heterogeneous cell signaling activity. The rationale is that if we identify what distinguishes more mature hPGCLCs from less mature ones and other cell types that arise at the same time, we can understand defects in their differentiation in vivo and in vitro and create better hPGCLCs. Our hypothesis will be tested through two specific aims: 1) Determine the combinatorial signaling dynamics responsible for hPGCLC induction by single cell tracking of signaling and fate markers in live cells combined with highly multiplexed immunofluorescence. 2) Determine if there are distinct phases of induction and maintenance and elucidate the signaling logic and gene regulatory network that controls hPGCLC maintenance and maturation. Our approach is conceptually innovative by testing if a unique history of signaling determines hPGCLC fate, by accounting for the interplay between exogenous and endogenous signaling in vitro, and by delineating clearly distinct phases of differentiation that start with induction. More generally we are breaking new ground by taking a systems-level approach to human germ line biology that tests hypotheses rigorously and quantitatively by representing them as mathematical models. The proposed work is also experimentally innovative as we use substrate micropatterning to achieve reproducible hPGCLC differentiation and are the first lab to establish long-term high throughput tracking of differentiating pluripotent stem cells as well as the first to adapt multiplexed immunofluorescence to stem cell models of early development. The expected outcome of our work is better fundamental understanding of human germ line differentiation and improved methods to produce hPGCLCs for research of in vitro gametogenesis.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Zika virus (ZIKV) is a re-emerging mosquito-borne flavivirus of significant public health concern. To date there are no effective licensed antiviral treatments or a vaccine. Therefore, elucidating the molecular biology of these viruses and the interactions with the host cell are foundational to identifying and developing effective treatment options. The single-stranded positive-sense RNA genome of ZIKV mimics a cellular mRNA. Specifically, the viral RNA encodes a single open reading frame, has structured untranslated regions (UTRs) adjacent to the open reading frame, and contains a N5’-methyl guanosine cap. Unlike mRNAs however, flaviviruses lack a poly(A) tail. From a multiple sequence alignment of all mosquito-borne flaviviruses we identified conserved regions containing 3-6 tandem adenosines in the 3’ UTR. These A-rich regions are localized in single-stranded regions within and between the XRN-1 resistant pseudoknots (xrRNA), dumbbell and 3’ stem loop (3’SL) RNA structures. In preliminary experiments we investigated the role of the A-rich region between xrRNA2 and the pseudo- dumbbell RNA structure (pre-pseudo/Y-dumbbell). Specifically, we generated three different mutations in a ZIKV Renilla luciferase reporter replicon and infectious clone. These mutants revealed that the pre-YDB A-rich region had a role in translation in both mammalian and mosquito cell lines. Different mass spectrometry studies have shown that the cellular poly(A) binding protein (PABP) interacts with the ZIKV 3’ UTR. Additionally, PABP was previously shown to interact with a region in the dengue virus 3’ UTR that harbors an A-rich motif. In preliminary studies we find that depletion of PABP1 decreased ZIKV, but not cellular, protein levels and viral titers without affecting cell viability. We therefore hypothesize that A-rich regions in the ZIKV 3’ UTR function to recruit cellular RNA binding proteins such as PABP1 to promote distinct steps in the virus infectious cycle. In Aim 1 we will mutate the A-rich regions in the infectious clone and a subgenomic luciferase reporter replicon to investigate the function of select A-rich regions on translation, replication, and viral fitness in mammalian and mosquito cells. In Aim 2, we will investigate the role of PABP1 on ZIKV gene expression and determine if PABP1 and other cellular RNA binding proteins bind A-rich regions in the ZIKV 3’ UTR. Overall, this study will advance our understanding of how flavivirus 3’ UTRs interact with the host to promote distinct steps in the infectious cycle in two vastly different hosts. Understanding how specific sequences in RNA genome function could lead to the therapeutic advancement namely the development of an attenuated vaccine ZIKV strain. Moreover, defining similar and unique RNA-protein interactions between mammalian and mosquito hosts could inform future vector control strategies.

National Institutes of Health

This Notice of Funding Opportunity (NOFO) solicits cooperative agreement research applications to support a multidisciplinary program titled "Accelerating Product Excellence in Innovation and for Clinical Adoption" (APEx), that will facilitate advancement of promising strategies and products for tissue engineering and regenerative medicine (TE/RM). APEx will be composed of Resource Centers (RCs) and associated Interdisciplinary Translational Projects (ITPs) in the area of therapeutics (including adult stem cell-based treatments), sensors, and diagnostics. RCs will capitalize on their available clinical, scientific, industrial, regulatory and commercialization expertise, to deliver technical support, research capacity, administrative infrastructure and regulatory and commercialization support to the ITPs and guide them to complete pre-clinical studies toward initiation of clinical trials. During this funding cycle, APEx will complete validation, manufacturing, and preclinical testing of the most promising products, which may include, but are not limited to products for detecting or treating tissue damage caused by congenital defect, traumatic injury, or chronic disease. Products that support early detection of chronic pathologies, monitoring of validated biomarkers of health or disease, as well as approaches to reduce or prevent resulting damage, are especially encouraged. The outcome of APEx will be TE/RM products with their regulatory approvals in place for first-in-human studies, along with associated clinical study protocols, and synthesis and manufacturing protocols ready for initiation of clinical trials.

NIGMS - National Institute of General Medical Sciences

PROJECT SUMMARY/ABSTRACT Clemson University’s rapid growth in externally funded research has propelled it to R1 status, reflecting its expanding impact in advanced scientific inquiry. Five of Clemson’s nine academic colleges are STEM-fo- cused, encompassing over 30 academic units. In the last decade, Clemson’s NIH-funded portfolio has grown from $5.5 million in 2014 to $26 million in 2024, currently spanning 85 awards across 57 investigators. This growth is fueled by the university’s strategic investments in research infrastructure, equipment, and facilities. These actions foster a resource-rich environment capable of attracting and retaining top research talent. Three major NIH Centers of Biomedical Research Excellence (COBRE) underscore Clemson’s priorities: the Eukaryotic Pathogens Innovation Center (EPIC), the South Carolina COBRE for Translational Research Improving Muscu- loskeletal Health (SC-TRIMH), and the Clemson University Center for Human Genetics. To further strengthen Clemson’s research capabilities, we seek to acquire a Refeyn mass photometer, a transformative technology that enables single-particle mass measurements. Unlike bulk methods such as dynamic light scattering (DLS), mass photometry quantifies molecular mass, providing an unparalleled view of heterogeneity, oligomerization states, and binding interactions at the single-molecule level. This technology is valuable across disciplines and research foci on campus, from probing protein-ligand and protein-protein inter- actions that occur in eukaryotic pathogens (EPIC) to evaluating biomolecular assembly and integrity in mus- culoskeletal research (SC-TRIMH). Investigators in human genetics can rapidly assess protein-DNA/RNA interactions and more complex heterogenous multi protein-protein-DNA/RNA complexes. The Refeyn mass photometer offers remarkable advantages: (1) Minimal sample requirement—only a few microliters of material are needed; (2) Low per-sample cost, approximately $2, making it accessible to both established laboratories and student trainees; (3) Ease of operation, a simple pipetting step onto a glass slide significantly reduces technical barriers; and (4) Broad applicability, it excels in characterizing oligomeric states, monitoring antibody binding, and confirming molecular compositions in diverse sample types. By installing this mass photometer at Clemson, we will foster interdisciplinary collaboration, enrich hands- on learning opportunities, and expand the capabilities of ongoing NIH-funded projects. Moreover, this cutting- edge instrument will position Clemson researchers at the forefront of next-generation single-particle analytics, supporting a range of studies—from early discovery to late-stage translational research. Although it also inte- grates seamlessly into cryo-EM workflows, the mass photometer’s utility extends well beyond structural biology. Ultimately, this S10 instrumentation request will allow Clemson to elevate its research enterprise, amplify productivity, accelerate innovation, and strengthen the university as a leader in biomedical and research.