University Of Washington

NIH Research Projects · FY 2026 · 2026-04

This K24 mid-career investigator award in patient-oriented research is to support the mentoring, research, and career development activities of Dr. Jillian Pintye, a nurse-scientist and Associate Professor at the University of Washington. The proposed mentoring and research aims are grounded in her work on HIV/STI prevention in pregnancy and will provide protected time to increase the number of clinician scientists mentored by Dr. Pintye. The overall goal of this proposed K24 is aligned with Dr. Pintye's mission to prepare the next generation of scientists with patient-oriented research experiences and skills to advance HIV/STI prevention among pregnant women—a unique and important priority population for STI/HIV research. Her combined leadership roles and five ongoing NIH-funded studies enable her to build a rich mentoring environment with opportunities for patient- oriented research among pregnant people and adolescent girls and young women affected by HIV and STIs. This K24 application proposes to sustain and grow Dr. Pintye's successful mentorship program and will leverage educational, career development, and research support programs available through the University of Washington and its highly productive and supportive HIV/STI research centers. She currently mentors several multidisciplinary clinician-scientists in a variety of clinical and public health fields including nursing science, infectious diseases, pediatrics, obstetrics and gynecology, clinical epidemiology, and implementation science. The K24 Mentoring Plan aligns with Dr. Pintye's mission to grow patient-oriented research in HIV and STIs among pregnant people by mentoring multidisciplinary trainees from the United States, Botswana, and Kenya. Mentees will gain experience in patient-oriented clinical epidemiology and implementation science research in pregnant women with primary mentorship from Dr. Pintye complemented by mentorship from collaborators in Botswana and Kenya. The proposed research aims are designed to provide evidence for HIV/syphilis elimination programs for pregnant women. Aim 1 will determine syphilis burden and clinical outcomes among pregnant women affected by HIV by leveraging clinical epidemiology data from (2) large ongoing RCTs in Botswana and Kenya. Aim 2 will assess clinical and implementation outcomes of incorporating syphilis testing at delivery in a pilot evaluation in maternity wards in Kenya and contribute preliminary data to design a future large-scale hybrid effectiveness-implementation RCT. Aim 3 will gather patient and provider perspectives on root causes of missed opportunities for maternal syphilis testing and treatment. In combination, these studies will contribute key evidence toward syphilis elimination and provide opportunities to develop diverse skills in patient-oriented research. The overall goal of the proposed K24 research aims is to inform policy and clinical practice for pregnant women affected by syphilis and HIV while training patient-oriented researchers. The K24 Career Development Plan includes formal mentorship, leadership, and research training in qualitative research, antenatal syphilis, and directing productive research centers to increase the impact of Dr. Pintye's research and mentorship.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY/ABSTRACT Cholera outbreaks have become larger and more frequent due to humanitarian disasters, rising antimicrobial resistance, and expanding Vibrio cholerae environmental reservoirs in warming oceans. The development of new, non-antibiotic interventions to treat cholera and prevent symptomatic disease is hindered by a lack of knowledge about why some people exposed to V. cholerae have mild symptoms and others develop severe dehydrating disease. The intestinal microbiota is a modifiable host factor that is known to impact clinical outcomes in enteric infections, yet the role of host microbes in the severity of human cholera is unknown. Our prior work established that host microbes (measured in stool) predict susceptibility to cholera, and our downstream studies found that this model successfully identified a gut bacterium that modifies host colonization with V. cholerae. Here, we propose to use these tools and methods to determine how intestinal microbes impact the severity of cholera in humans. We approach this question by studying emesis, which is generated in the upper intestine during cholera, rather than studying the stool microbiota. We propose using emesis because V. cholerae is a small intestinal pathogen that colonizes and expresses cholera toxin in the upper intestine. The microbiota of the upper intestine differs from that measured in stool, because there is a higher oxygen tension and distinct microbial communities in the upper intestine compared to the rectum, where stool is formed. The goal of this study is to characterize the upper intestinal microbiota during human cholera and define the mechanisms by which host microbes impact the severity of cholera. By comparing the upper intestinal microbiota of people with mild to moderate cholera to those with severe disease, we will test how host microbiota impacts V. cholerae in the upper intestinal environment. The overall objective of this study is to understand how the upper intestinal microbiota impacts the severity of human cholera. Our central hypothesis is that upper intestinal host microbes modulate V. cholerae virulence factor expression. The rationale is that cholera emesis reflects the upper intestinal environment; therefore, emesis is more likely to contain gut microbes that interact with V. cholerae during active infection. We will test our hypothesis using two specific aims: 1) Define the cholera-specific upper intestinal microbiota, and 2) use emesis- derived bacterial isolates to define gut microbe-V. cholerae interactions. The proposed work is innovative because we will use emesis rather than stool to study the relevant host microbiota. This study is significant because we will gain foundational knowledge about clinically relevant host microbiota-enteric pathogen interactions. These results may impact human health by establishing a foundation for using commensal microbes as probiotics to reduce V. cholerae virulence, and ultimately to prevent symptomatic cholera or shorten the duration of disease.

NIH Research Projects · FY 2026 · 2026-04

Project summary My long-term career goal is to reduce the influenza burden by promoting data-driven and evidence-based influenza policies. My short-term goal is to address the role of vaccines’ antigenic match in mitigating influenza burden and to optimize vaccine strain selection process using genetic surveillance data. The proposed training and research program will position me to become an independent investigator and establish my research group at the intersection of influenza epidemiology, health policy, statistics, and decision science. Candidate: My background in health decision science has equipped me with training and research experience in comparative effectiveness and simulation modeling of infectious diseases. However, I lack methodological skills necessary to infer the effect of improving antigenic match on the risk influenza complications in real-world data and to assess the value of genetic surveillance data for better antigenic match. The training proposed in this K01 award will build on my background and provide me with the skills I currently lack to conduct the proposed research. Training plan: This plan includes formal coursework, workshops, seminars and personal mentoring. I will dedicate 75% effort to the training and research activities proposed, under the supervision of my primary mentor Dr. Anirban Basu. Dr. Janet Englund, Dr. Trevor Bedford, and Dr. Adam Szpiro will be my co-mentors. Dr. John Huddleston, Dr. Matthew Biggerstaff, and Dr. Richard Zimmerman will serve as advisors, and Dr.Vanja Dukic will be a collaborator. My specific training goals are: 1) To learn and implement spatio-temporal data analysis and visualization methods; 2) To develop an in-depth understanding of influenza virus evolution and incorporate it into an epidemiological model; 3) To learn value-of-information analysis in the context of using genetic surveillance for vaccine strain selection; 4) Engage with the influenza policy community and stakeholders; and 5) Improve my grant writing skills and submit an R01 grant application. Research plan: The overarching theme of this K01 research program is to improve the outcomes of seasonal influenza vaccines through enhanced genetic surveillance. My specific aims are to 1) Describe the spatio- temporal patterns of the vaccine antigenic match, vaccine uptake, and influenza health outcomes; 2) Estimate the real-world impact of enhancing the influenza vaccine’s antigenic match on influenza-related hospitalizations and deaths; and 3) Estimate the net benefit of collecting additional genetic sequencing data of influenza viruses in the surveillance system to improve vaccine strain selection. Impact: The findings from the proposed research will offer opportunities to better prepare for influenza seasons with low antigenic coverage and optimize resources allocation for influenza vaccine composition, enhancing the influenza surveillance landscape.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY Acetaminophen, which is found in more than 600 prescription and non-prescription medications for mild to moderate pain and fever reduction, is not restricted to pharmacies and is sold over-the-counter in many countries, including the United States. In most populations worldwide, over 50% of pregnant people report taking acetaminophen, which easily crosses the placenta and fetal blood brain barrier, potentially affecting fetal brain development. The United States Food and Drug Administration (FDA) and European Medicines Agency (EMA) have traditionally viewed acetaminophen as posing minimal risks to the fetus when used as directed but have called for more rigorous studies and better safety data to inform their recommendations on how pain medicines are used during pregnancy. Accumulating evidence from epidemiologic and animal research highlights potential neurodevelopmental risks associated with prenatal acetaminophen exposure, yet limitations remain in the literature preventing regulatory agencies from assessing whether these associations are causal. Prior studies could be confounded by genetic or familial factors, and mechanisms linking acetaminophen with adverse neurodevelopment remain unknown, limiting our ability to develop targets for harm reduction. While adjusting for a robust set of genetic, environmental, and familial factors, this proposal aims to elucidate molecular mechanisms and genetic effect modifiers of associations between prenatal acetaminophen and adverse neurodevelopment. During the mentored K99 phase, I will receive training from leaders in pediatrics, child psychiatry and psychology, pharmacogenomics, metabolomics, and multi-omics. I will combine this training with my prior expertise in prenatal acetaminophen research and epidemiology to model associations of maternal blood biomarkers of acetaminophen with a broad spectrum of child neurodevelopmental outcomes, including ADHD. I will investigate genotype by prenatal acetaminophen interactions on child neurodevelopment (K99 Aim 1) and conduct a Metabolome-Wide Association Study (MWAS) of prenatal acetaminophen exposure (K99 Aim 2) in a single site study. Genetic expertise gained from the K99 training and Aim 1 will enable me to explore genotype by prenatal acetaminophen interactions in a meta-regression analysis of multiple cohorts (R00 Aim 3), which will require advanced methods accounting for heterogeneity in allelic effects by ancestry. Metabolomics and multi-omics expertise gained from the K99 training and Aim 2 will enable me to conduct MWAS in this multi-cohort setting, and employ multi-omics pathway integration to uncover biological pathways altered by prenatal acetaminophen (R00 Aim 4). Through this K99/R00 award, I will gain subject matter expertise in developmental psychopathology and molecular analytic skills in precision medicine, pharmacogenetics, metabolomics, and multi-omics. These research and training opportunities will prepare me to lead an independent lab harmonizing omics and epidemiologic approaches to study molecular mechanisms linking prenatal exposures with neurodevelopment.

NSF Awards · FY 2026 · 2026-04

Learning is central to both human life and artificial intelligence. People learn to move, communicate, reason, and recover skills after injury, yet how the brain achieves this learning remains poorly understood. This project studies how neurons in the brain change their coordinated firing activity during learning and how that knowledge can be used to guide learning to proceed faster and more effectively. The work focuses on the primary motor cortex, a brain region involved in the control and learning of movement. The project will investigate how neural circuits change over hours versus days of learning. By revealing the mechanisms that support learning in the brain, this project may inform new strategies for neurorehabilitation after injury or disease, improve methods for guided skill training, and inspire more robust, efficient, and interpretable artificial intelligence systems that learn more like biological brains. The project also advances education and workforce development by integrating research with modernized university training, publicly available online mini-courses, classroom outreach for middle and high school students, and public-facing science communication. The project will combine computational modeling with experimental data from monkeys performing brain computer interface learning tasks that probe multiple timescales of learning. It will test the hypothesis that rapid learning primarily reflects changes in the inputs that drive a population of neurons, whereas slower but more flexible learning reflects changes in local recurrent circuitry within that population. First, the project will develop recurrent neural network models to determine how these candidate circuit-level mechanisms can reshape neural population activity and behavior. Second, the project will develop machine learning methods to infer which learning mechanisms best explain recorded neural activity in primary motor cortex during short-term and multi-day learning. Third, the project will use these models to design individualized training curricula and neural interfacing protocols intended to accelerate learning by guiding neural activity along more effective paths. Together, these activities will establish a framework for identifying circuit-level mechanisms of learning, testing how those mechanisms constrain or enable behavioral change, and using that knowledge to guide learning in both biological and engineered systems. This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY/ABSTRACT Each year, over 100,000 patients in the US are diagnosed with favorable-risk prostate cancer for which clinical guidelines recommend active surveillance. Active surveillance (AS) involves cancer monitoring with clinical tests such as serum prostate specific antigen (PSA), prostate biopsies, and magnetic resonance imaging (MRI), such that definitive treatment (e.g. surgery or radiation) is delayed until signs of unfavorable cancer are evident, or treatment is avoided altogether. While the majority of men on AS will remain free of progression for more than 10 years, about 20% of cancers that appear low risk at diagnosis progress to aggressive phenotypes (grade group >3 cancer, recurrence after treatment, or metastasis). Early identification of these aggressive cancers will allow for earlier treatment, at a time when treatment may be curative. Although several biomarker tests have been developed and validated to improve prediction of higher risk disease after primary treatment, there are no biomarker tests that have been validated for clinical use in the large population of men on AS. The Canary Prostate Active Surveillance Study (PASS), established in 2008, is the only prospectively accrued, multi-institutional cohort of men on AS in North America. PASS has 2,300 participants with a median follow-up of 8 years. Extensive clinical, imaging (e.g. MRI), epidemiological data and longitudinal biospecimens are collected according to a standardized protocol. In this proposal, we will use the Canary PASS cohort to interrogate novel radiomic, pathomic, and liquid biomarkers for early identification of cancers that progress to aggressive disease. The overall goal of the proposed research is to develop a predictive tool that will accurately identify patients initially diagnosed with favorable-risk cancer that will progress to aggressive cancer better than routine clinical, pathologic, and imaging data. We will accomplish this goal using the following Aims: 1) Interrogate PSA isoform biomarkers for their ability to predict aggressive disease in patients using AS. We will leverage data from existing and emerging collaborations to evaluate if isoforms of PSA improve prediction of aggressive disease compared to the clinical standard of total PSA. 2) Interrogate MR imaging biomarkers for their ability to predict aggressive disease in patients using AS. We will A) evaluate whether computer-aided diagnostic (CAD) in a commercial, FDA cleared artificial intelligence (AI)-derived MRI platform detects aggressive cancer, B) develop and validate an AI-based radiomic biomarker for prediction of aggressive disease in patients on AS. 3) Interrogate histopathology signatures for improved prediction of aggressive disease in patients using AS. We will A) evaluate outputs from a commercial AI histopathology tool for prediction of aggressive cancer, B) develop and validate an AI-derived histopathology signature trained for prediction of aggressive disease in patients on AS. Secondary Aim: Develop a decision rule for incorporating multiple biomarkers and clinical data for optimal prediction of aggressive prostate cancer in patients using AS.

NIH Research Projects · FY 2026 · 2026-04

Polygenic Risk Scores (PRS) developed from analysis of large-scale genomic data in epidemiological studies hold promise as a precision medicine tool that will help identify individuals at higher disease risk. However, a critical challenge now facing PRS research and clinical translation is that most PRS have been developed using data from individuals in limited populations, resulting in poorer predictive performance across populations and reflecting the lack of representation of genetic variation in genomic and biomedical research more broadly. NHGRI is establishing a new Polygenic Risk Score Methods Development Consortium to address this challenge by (1) leveraging existing cohorts to improve PRS prediction across populations and for a range of conditions and (2) optimizing the integration of large-scale genomic and phenotype datasets in support of collaborative analysis, reporting, and creation of methods and resources for the broader scientific community. As Coordinating Center, we will support the Consortium's goals by achieving four main aims: (1) leading harmonization of genotype and phenotype data across Consortium Study Sites and Affiliate Members, including variant and sample level quality control, genotype imputation, and use of standard phenotype ontologies. (2) Organizing cross-Consortium analysis and collaborative methods development, featuring standardized evaluation of PRS methods to identify consensus approaches, development of a local-ancestry informed PRS method, and integration of ELSI considerations into analytic best-practices. (3) Facilitating data sharing within and beyond the Consortium through community resources and repositories such as the NHGRI Genomic Data Science Analysis, Visualization, and Informatics Lab-space (AnVIL), NCBI database of Genotypes and Phenotypes (dbGaP), and the Polygenic Score Catalog. (4) Coordinating program logistics and outreach including through a Consortium website, in-person meetings, mentorship and training, and regular engagement with precision medicine partner programs. We propose innovative approaches to achieve these four main aims, including leveraging emerging cloud-based platforms for harmonization, analysis, and sharing of large-scale genomic data; investigating scalable data science approaches to phenotype harmonization; leading a Consortium-wide “bake-off” to establish consensus approaches to PRS generation and evaluation; and incorporating Ethical, Legal, and Social Implications into analytic best practices. Furthermore, our application rests on 13 successful years of experience and expertise serving as Coordinating Centers for five large-scale genetic and biomedical projects. Through scientific and administrative leadership of this Consortium, we will help realize the public health benefit of developing PRS that predict and help prevent or mitigate a range of diseases.

NIH Research Projects · FY 2026 · 2026-04

ABSTRACT Millions of Americans each year experience adhesion-related small bowel obstruction (aSBO), a condition associated with significant morbidity and prolonged hospitalization. Adhesions formed after previous abdominopelvic surgery can cause twisting of the bowel resulting in injury and a cascade of inflammation that results in progressive bowel wall edema with narrowing of the bowel lumen. This can lead to or worsen the bowel obstruction. Evidence from both clinical practice and animal models suggests that reversing this inflammation can hasten the return of bowel function and avoid surgery for people with aSBO. For example, intravenous dexamethasone is effective in avoiding surgery in patients with a form of SBO related to malignancy (malignant ascites or metastatic disease). A Cochrane review evaluated three RCTs and found “evidence that dexamethasone…may bring about the resolution of bowel obstruction”. An underappreciated aspect of these RCTs is that almost all patients had a history of abdominopelvic surgery. Since it is difficult to distinguish the extent to which an SBO is caused by adhesions from prior surgery or mass effect related to malignant ascites or metastases, we hypothesize that dexamethasone may be efficacious in resolving aSBO as well. The proposed, Comparison of Outcomes of Management of Bowel Obstruction (COMBO) trial is a double-blinded randomized study of a short course of dexamethasone + supportive care vs. placebo + supportive care. The primary outcome is non-operative resolution of aSBO without major complications as defined using modified National Surgical Quality Improvement Program (NSQIP) criteria. Secondary outcomes–clinical, healthcare utilization and patient- reported outcomes–will be compared overall and across subgroups (e.g., based on severity of aSBO, number of prior aSBO events, sex). Reducing inflammation with dexamethasone–a readily available and safe intervention–may improve the likelihood of non-operative management of aSBO and could change the management of millions of patients with this condition.

NIH Research Projects · FY 2026 · 2026-04

Project Summary. Nucleoside analogs are an important class of pharmaceutical compounds that serve as the cornerstone for antiviral therapy. Beyond viral infections, various nucleoside analogs have also shown antitumor, antibacterial, antifungal, and herbicidal activity. Though synthetic chemists can design new nucleoside analogs de novo, a large fraction of our pharmaceuticals are inspired by bioactive compounds made by bacteria. The proposed work will investigate the biosynthesis of a cryptic family of natural product nucleoside analogs that contain ‘rare’ functional groups. This work will be enabled by the research group’s expertise on non-standard nucleoside biochemistry, chemical biology, genetics, and analytical chemistry. Initial work will combine genetic engineering with comparative genomic/comparative metabolomics to identify key enzymes involved in halogenation and sulfamate formation. Since these perform valuable transformations, they make promising candidates as biocatalysts for pharmaceutical synthesis. Notably, kinetic and substrate/reaction characterization of these enzymes will be explored test the feasibly of using these enzymes for alternative synthesis of existing nucleoside analog therapeutics. As a subsequent goal, this work will also explore how ‘modular’ biosynthesis of these nucleoside natural products can be used to rapidly synthesize inhibitors of a wide-range of enzymes. Key innovations here will include combinatorial assays with ribozyme components. Finally, this work will look to integrate bioinformatic/metabolomic/genetic approaches to discover unknown nucleoside analogs made by various bacteria. Specifically, we highlight existing evidence of hybrid gene clusters that make unknown nucleosides. As a general vision, this research program poses that elucidating nucleoside biosynthesis pathways, characterizing enzymes that perform rare biochemistry, and discovering new bioactive nucleosides will expand the repertoire of biocatalytic tools available for making life-saving nucleoside analogs.

NIH Research Projects · FY 2026 · 2026-04

Summary Mitochondria are released by dying neutrophils in peripheral blood and tissue, contributing to inflammation and organ damage. Little is known about mechanisms to clear the extracellular mitochondria. Neutrophils can generate, and release, complement C3, an important opsonin in removal of cell debris. However, whether neutrophils can proteolytically activate C3, and the role of C3 in clearance of mitochondria is not known. The aim of the present study is to explore mechanisms of mitochondrial clearance, with a focus on the role of neutrophils in proteolytically opsonizing mitochondria with complement C3b, and consequences of C3b in downstream clearance of mitochondria by myeloid cells. The premise is that neutrophils, through proteolytical cleavage, opsonize mitochondria with C3b facilitating their clearance while limiting inflammation and tissue damage. To investigate this, we have two main aims. The first aim investigates mechanisms related to complement C3 release and proteolytic cleavage by neutrophils. Neutrophils from patients (n=40) and controls (n=20) will be analyzed for C3 content by qPCR and flow cytometry. The identify of the C3-cleaving protease(s) will be identified using select protease inhibitors in neutrophils, supernatants and isolated NETs. Binding of C3 to mitochondria will be characterized using immunoprecipitation, mass spectrometry, and fluorescence microscopy. The second aim investigates the role of complement C3 in mitochondrial clearance, both in vitro and in vivo. In vitro, the role of C3 in opsonizing mitochondria will be determined in myeloid cells assessing uptake, induction of inflammatory cytokines, as well as NET formation by neutrophils. In vivo, GFP- tagged mitochondria will be injected in WT or C3-/- mice and assessed for biodistribution over time using confocal microscopy. At the completion of this proposed research, our expected outcomes are to have identified novel mechanisms regulating complement C3 release and acitvation by neutrophils. Further, we anticipate to have identified key pathways involved in mitochondrial clearance, and its implication for downstream effector functions in recipient cells. We expect this work to have a positive impact because it will offer novel insight into basic neutrophil biology, as well as identify targetable pathways to limit mitochondrial- mediated inflammation and subsequent organ damage in SLE.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY Over 1.4 million individuals in the United States are diagnosed with Lewy Body Dementia (LBD), the second most common type of degenerative dementia after Alzheimer's disease (AD). LBD results in early impairments in cognitive abilities, along with bothersome neuropsychological and bodily symptoms such as visual hallucinations, parkinsonism, dysautonomia, and sleep disorders. Up to 80% of individuals with LBD receive care from family members, with nearly half of the caregivers' experiencing depression. Web-based and telehealth interventions for caregivers of individuals with dementia are promising solutions for reducing caregiver depression, paralleling the potential of traditional in-person approaches. Yet, most of the interventions generalize across all dementia forms without adaptations for LBD's distinct challenges. Accessibility of existing digital interventions is also limited by internet bandwidth and lower digital literacy in caregiving populations, perpetuating inequity and leaving them underserved. Our project aims to test the effectiveness of a fully asynchronous, low bandwidth, text-based psychoeducational online intervention tailored specifically for caregivers of individuals with LBD (VOCALE LBD). This intervention engages caregivers in moderated peer-to-peer discussions focused on LBD caregiving and problem-solving skills over an eight-week period. In a pilot study, the intervention showed promising results in reducing depressive symptoms among fifty-four LBD family caregivers age 68±10. Clinicians also uniformly agreed that the intervention is impactful, acceptable, and well-aligned with their strategic priorities, but they suggested strengthening its pragmatic potential by introducing practical measurements of the intervention's progress. We propose a two-arm randomized controlled trial (RCT) comparing VOCALE LBD to the standard of care (SOC) among 220 caregivers nationwide, recruited using Lewy Body Dementia Association (LBDA) outreach. The primary outcome will be depressive symptoms at eight weeks post-enrollment. Secondary outcomes will include sustained effects on depressive symptoms at six months, and exploratory outcomes will assess caregiving burden, stress, social support, and loneliness. Additionally, we will evaluate the mechanisms influencing the intervention's effects, focusing on caregiver empowerment and problem-solving, and explore pragmatic approaches for monitoring the intervention's effectiveness through user engagement and user-generated data. Our project is aligned with national priorities to effectively leverage digital and telehealth solutions for caregivers of people with Alzheimer's Disease and Related Dementias (ADRD). We aim to create an evidence- based, equitable, and accessible solution for LBD caregivers, ensuring practical application and intervention fidelity. If successful, this project will lay a foundation for the next stage effectiveness research in clinics and community organizations.

NIH Research Projects · FY 2026 · 2026-03

SUMMARY/ABSTRACT Inflammatory bowel disease (IBD) is an autoimmune condition which leads to symptoms of abdominal pain and diarrhea. In women with IBD, symptoms (e.g., abdominal pain and diarrhea) vary with their menstrual cycle phase, however, there is limited clinical data linking estrogen or progesterone fluctuations to systemic or localized gut inflammation. Our project aims to reduce this gap in knowledge by testing the relationships between estrogen levels and systemic indicators of inflammation (e.g., cytokines, CRP) as well as gastrointestinal (GI)-specific markers (i.e., fecal calprotectin, bowel wall thickness) among women with IBD. We will also describe important patient-reported outcomes including daily symptoms and life interference, quality of life. The study design accounts for the impact of two distinct phases of the menstrual cycle (mid- luteal vs. menses) and compares those with IBD to healthy controls (HCs) and those with a disorder of gut- brain interaction (DGBIs) (n=50 per group). Participants will track their menstrual cycle and will complete daily symptom reports. The specific aims are: 1) To compare systemic (i.e., cytokines, CRP) and GI-specific (i.e., fecal calprotectin) inflammatory markers and patient-reported outcomes (i.e., symptoms, quality of life) in females across IBD, HCs, and DGBI groups and between mid-luteal and menses phases; 2) To determine the relationship between estrogen and systemic and GI-specific inflammatory markers, and patient-reported outcomes during mid-luteal and menses phases across IBD, HCs, and DGBI groups; 3) (a) To evaluate bowel wall thickness between mid-luteal and menses phase and (b) to determine the relationship between estrogen levels and bowel wall thickness across IBD, HCs, and DGBI groups. Better understanding the impact of the menstrual cycle on systemic and GI-specific inflammation and patient-reported outcomes in IBD is the first foundational step needed to realize our goal improving the health of women with autoimmune conditions.

NIH Research Projects · FY 2026 · 2026-03

Project Summary Energy-intensive behaviors demand high oxygen supply, presenting a fundamental physiological challenge across the animal kingdom. Respiratory organs have evolved diverse forms - from insect spiracles to fish gills to human lungs. Yet their neural control systems serve a conserved purpose. They need to actively monitor respiratory gases and regulate both gas exchange and energy consumption during behavior. The neural mechanisms coordinating respiration with behavior remain poorly understood. In particular, we know little about how respiratory circuits interact with motor control systems during varying metabolic demands. Here I propose to investigate the neural basis of respiratory control during behavior. I have made two important discoveries that uniquely position me to investigate the neural control of respiration. I have identified the complete set of motor neurons controlling respiration in flies, and I have discovered novel gas- sensing neurons in muscles and respiratory tracts that detect respiratory state and modulate behavior. I have made genetic drivers that label both populations of neurons. With these advantages, I will investigate three fundamental aspects of respiratory control by combining genetics, connectomics, behavioral tracking, and in vivo imaging. First, I will examine the neuromuscular basis of respiratory control during locomotion. Second, I will investigate interoceptive mechanisms of respiratory gas sensing. Third, I will study the neural integration of respiratory and metabolic signals. This work will reveal how animals optimize respiratory control while maintaining homeostasis during behavior. The principles uncovered in this tractable system will provide an experimental and conceptual framework for studying respiratory control across species. My long-term goal is to establish an independent research program on neural control of respiration and energy homeostasis. The research and career development in this proposal will provide essential experimental, theoretical, and mentorship training. To support my transition to independence, I will be co-mentored by two experts at the University of Washington: Dr. John Tuthill, an expert on sensorimotor control in flies, and Dr. Jan-Marino Ramirez, an expert on mammalian respiratory control.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY/ABSTRACT During development, neurons that are generated at a single location can go on to innervate different targets and carry out different functions. A fundamental question in developmental neurobiology is to understand how this functional diversification occurs. The developing brainstem gives rise to facial branchiomotor neurons (FBMNs), which innervate different sets of muscles in the face and collectively control all facial movements. While the developmental programs specifying FBMNs are well understood, differences between FBMNs that enable them to wire to different upstream neurons and muscle targets to control different behaviors remain poorly understood. Agenesis, miswiring, and other developmental anomalies of FBMNs cause Congenital Cranial Dysinnervation Disorders (CCDDs), characterized by clinical presentations including facial paralysis, depending on which neurons are affected. A better understanding of FBMN development will also advance our understanding of the etiologies of CCDDs. The evolutionary conservation of FBMNs enables investigation in the transparent zebrafish embryo. To identify transcriptional heterogeneity among developing FBMNs, single-cell RNA sequencing and in situ hybridization were used, identifying two transcriptionally distinct populations in the facial motor nucleus, the brainstem structure composed of FBMN cell bodies. The positions of the two transcriptional populations correlate with developmental age: earlier-born neurons migrate to ventral positions and express different genes than later- born neurons, which migrate to dorsal positions. While previous studies have identified some topography in the facial motor nucleus, the relationship between topography, birth order, and gene expression remains unclear. These observations raise the possibility that birth order specifies distinct gene expression programs, which specify innervation targets. Aim 1 proposes to use high-resolution live imaging to uncover the organization of the facial motor nucleus and determine whether this organization is a product of developmental timing. Aim 2 proposes to combine rapid reverse genetic screening and multiplexed single-cell transcriptomic phenotyping to identify functional regulators of facial motor nucleus development, with specific insight into the etiology of the CCDD, Hereditary Congenital Facial Paresis.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY/ NARRATIVE Substance use disorder affects about 24 million people in the US due to the heightened availability of psychostimulants and synthetic opioids. Drug overdose deaths have also dramatically increased, requiring an urgent need to develop new therapeutics for this ongoing epidemic. Identifying how stress increases vulnerability to the reinforcing effects of drugs in susceptible individuals is important for developing effective strategies to treat SUD and mood disorders. Stress activates the release of the endogenous neuropeptide dynorphin (Dyn) that activates Gαi/o -coupled Kappa opioid receptor (KOR). Activation of KOR leads to the recruitment of the mitogen- activated protein kinase (MAPK), specifically p38α in addition to its canonical Gαi/o·Gβγ activity. KOR activation of p38α in serotonergic neurons (5HT) has been shown to mediate stress-induced potentiation of cocaine preference and increased serotonin transporter (SERT) function in the dorsal raphe nucleus (DRN). This increase in SERT activity is hypothesized to cause a hyposerotonergic state in the nucleus accumbens (NAc). In contrast, during morphine withdrawal, the hyposerotonergia is hypothesized to be a function of increased presynaptic inhibition of 5HT release by KOR. Thus, the mechanism by which KOR activation leads to hyposerotonergia remains to be resolved. Additionally, KOR activation of p38α in the ventral tegmental area (VTA) dopamine (DA) neurons is also required for aversion in mice, and pharmacological inhibition or selective gene deletion of p38α in VTA DA neurons blocks the aversive response to stress. Together, the Dyn/KOR system remains a potent modulator of both the 5HT and DA systems that regulate the stress response. Understanding how 5HT and DA dynamics are regulated by KOR/Dyn is an essential next step in the development of novel therapeutics for stress-induced mood disorders and SUD. Both Aims 1 and 2 of the proposal will characterize the pharmacological and behavioral role of stress-induced activation of Dyn/KOR/p38ɑ MAPK using in vivo fiber photometry with novel GRAB sensors and cell-specific CRISPR gene deletion to monitor real-time 5HT and DA tone in the NAc. These studies will be the first to offer high-resolution, simultaneous analysis of the 5HT/DA systems modulation during stress to describe 1) 5HT/DA sensitivity to p38α during both pharmacological and behavioral modulation, 2) the mechanism by which KOR G-biased agonists and antagonists may promote stress resilience, and 3) use dual-color imaging to understand 5HT/DA together during stress. These findings will provide foundational knowledge informing stress, neuropharmacology, and opioid fields.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY / ABSTRACT Monitoring neuronal activity modulation is pivotal for elucidating brain functionality and addressing neurological disorders. Despite the advancements brought by green fluorescent calcium indicators like GCaMP and neuromodulator sensors, a considerable gap persists in the development of red fluorescent sensors that match the properties of their green counterparts. This gap, characterized by limitations in dynamic range, photostability, and kinetics, restricts a more comprehensive exploration of neuronal interactions, especially in multiplexed, dual-imaging imaging scenarios. Additionally, the iterative engineering approach for new sensor development is notoriously slow and labor-intensive. Our central goal is to leverage our sensor screening platform, Opto-MASS, as well as our recent successes in using machine learning to expedite the optimization of fluorescent sensors. This project aims to engineer red fluorescent calcium and neuromodulator sensors that match the kinetics and dynamic range of green sensors and further enhance their properties. Our objectives include the rigorous benchmarking of these sensors against the best-in-class for properties such as dynamic range, kinetics, and photostability, followed by comprehensive in vivo validation across multiple laboratories and application scenarios using fiber photometry and two and 3-photon imaging. Our project is innovative because it utilizes a high-throughput screening assay capable of evaluating over 10,000 sensor variants from library collections in under an hour, a significant advancement over current methods. Coupled with pioneering machine learning models that identify key residues affecting sensor performance, we will significantly accelerate fluorescent sensor development, particularly for red calcium and GPCR-based sensors. Importantly, we aim to achieve these goals while reducing time and resource commitments. Our project directly addresses critical needs outlined in this FOA, including a broader range of reliable sensors in neuroscience research that facilitate nuanced, multidimensional studies of brain activity. By developing sensors with improved dynamic ranges, kinetics, and photostability, we aim to overcome existing barriers to multiplexed imaging of neuronal dynamics in vivo. Ultimately, the successful completion of this project would not only fill a vital gap in neuroscientific research tools but also align with the NIH BRAIN Initiative's objectives to advance neurotechnology and set new standards for molecular tool development and in vivo validation in neuroscience.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY Translating knowledge of the genetic basis of disease into better health outcomes is the major promise of translational genomic medicine and precision medicine. However, common, actionable genomic conditions with well-understood genetic components and effective early detection and treatment protocols, such as hereditary breast and ovarian cancer, Lynch syndrome, and familial hypercholesterolemia, are too often not detected by current screening protocols. Population-based genomic screening for all adults in primary care settings holds the promise of earlier identification of those at risk, leading to reduced morbidity and mortality through earlier monitoring, treatment, and other interventions. The Population Genomic Screening Network (PGSN) will pilot genomic screening in primary care settings for these and select additional genomic conditions. PGSN will recruit over 20,000 adult participants across diverse clinical settings, targeting health disparities populations. As the PGSN Coordinating Center, we will (1) coordinate and monitor the Network’s design and implementation of the screening program, including serving as the single IRB, coordinating consensus-driven development of a screening program implementation manual, monitoring and reporting on screening program implementation processes, and supporting the Network’s community engagement plan. We will also (2) manage and release the Network’s data, including coordinating and monitoring the secure transfer and management of data across the Network, developing a data model to support data aggregation and harmonization, and producing a cleaned, well-documented, de-identified Network dataset that will be released to the scientific community. We will also (3) contribute to the collaborative development and dissemination of best practice and lessons learned from the pilot program. Lastly, we will (4) provide comprehensive administration of PGSN’s logistics, communication, and governance including scheduling and managing all Network calls, organizing in-person/hybrid meetings, overseeing communications and calendaring, and hosting a comprehensive website.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY/ABSTRACT The goal of this proposal is to develop an ex vivo experimental platform to enable novel investigations into the roles of the intestinal lumenal and basal microenvironment on the origins of Crohn's Disease (CD). CD is a chronic, idiopathic inflammatory disease of the intestines whose incidence and prevalence are increasing in the U.S. and globally. The disease has a disproportionate impact on the health and well-being of CD patients as well as significant use of health care resources. CD is thought to result from a breakdown of immune tolerance due to a compromised mucus hydrogel and/or epithelial cell barrier function early in the disease, allowing the inappropriate ingress of lumenal microbiota and their metabolites into the basal tissue microenvironment. Prior experimental models of CD are limited by the use of non-human or tumor cells that do not reflect human intestinal physiology, organoid models that do not fully mimic tissue microarchitecture and cell organization, or monolayer systems on stiff surfaces that lead to stem/proliferative cell loss and altered differentiated cell properties. To resolve these limitations, an interdisciplinary collaboration with expertise in advanced bioengineered intestinal platforms, immunology, and clinical gastroenterology has been formed to construct a 3D intestinal platform incorporating primary intestinal and immune cells to support a microenvironment that correctly mimics the colon in health and Crohn’s disease. A physiologic patterned mucus hydrogel will act as a protective barrier and lubricating surface along the lumenal epithelial cell surface. A magnetic fecal surrogate comprised of cellulose and colonic bacteria will recreate the properties of colonic fecal material and its biophysical and biochemical interactions with the lumenal epithelial surface. Collectively these advances in tissue engineering of a humanized colon-on-chip will create an accurate biointerface to produce a powerful ex vivo system to investigate the complex interplay of the intestinal epithelium, mucus hydrogel, fecal microbes/biomatrix and immune cells in health and CD. As a cell source, the project will take advantage of an extensive biobank of over 1000 HLA-typed normal donors and CD patients comprised of paired primary intestinal immune cells and colonic epithelium established at the Benaroya Institute. These specimens will enable the use of autologous tissues to avoid the confounding effects of allogeneic immune reactions.

NIH Research Projects · FY 2026 · 2026-03

SUMMARY This project aims to address the high prevalence of frailty among independently living (IL) residents in Continuing Care Retirement Communities (CCRCs) through the development and evaluation of VOCALE, a scalable digital intervention. Nearly 700,000 residents across 2,000 CCRCs in the United States rely on these communities for levels of care from IL to skilled nursing. Frailty, affecting over half of these individuals, leads to increased vulnerability to adverse health outcomes and care level transitions. Existing multi-component interventions show potential in enhancing quality of life (QoL) for older adults but face barriers in CCRCs, such as limited space and staffing challenges, which impede effective implementation. The current focus in CCRCs on compensatory rather than preventive care in IL often limits resident engagement in proactive health management. VOCALE addresses these challenges with an eight-week web-based program designed for older adults with limited digital literacy. It offers low-bandwidth, asynchronous access to self-care resources, peer support, and problem-solving tools specifically designed to target frailty and improve QoL. Preliminary results from 28 CCRC residents aged 66-92 with frailty indicate VOCALE's feasibility and acceptability. Findings showed a clinically significant 10-point improvement in RAND-36 QoL scores, with large effect sizes in overall QoL and physical function and fatigue subscale improvements (0.5 and 0.8, respectively). Additional gains were observed in other health metrics with sustained engagement and low attrition rates of 20-25%. Building on these findings, we propose a confirmatory Stage II and exploratory Stage III trial to evaluate VOCALE's efficacy, mechanisms of action, and implementation potential within CCRCs. This eight-week, two- arm RCT with 128 frail residents across 10 CCRCs will randomly assign facilities to VOCALE or care-as-usual and will focus on the following aims: 1) To evaluate VOCALE's efficacy in improving QoL and reducing frailty in CCRC residents. Using a cluster-randomized design, we will measure QoL (primary outcome) and Fried's frailty measure (secondary outcome) post-intervention and one-month later; 2) To identify mechanisms through which VOCALE impacts QoL and frailty. We will assess empowerment, social support, and problem-solving skills as mediators, hypothesizing that these factors will mediate the relationship between VOCALE and observed outcomes; 3) To explore VOCALE's implementation potential in CCRCs using the CFIR framework to assess acceptability, feasibility, and organizational readiness for VOCALE's integration into CCRC workflows. Focus groups, interviews, and surveys with administrators and staff will provide insights into adoption, hypothesizing that VOCALE will be well-received with minimal resource demands. This project will provide critical evidence on VOCALE's capacity to fill an unmet need for scalable, preventive interventions that enhance the health, independence, and QoL of IL CCRC residents with frailty, with strong potential for widespread clinical and public health impact.

NIH Research Projects · FY 2026 · 2026-03

PROJECT SUMMARY/ABSTRACT Cirrhosis, the late-stage complication of liver disease, stands as a leading cause of death globally and frequently causes kidney dysfunction. Yet, the mechanisms leading to kidney function loss in cirrhosis remain incompletely understood, which in turn limits the development of effective therapeutic options. I have generated data showing subclinical injury to the proximal kidney tubules (PTs) in stable outpatients with cirrhosis irrespective of glomerular filtration rate (GFR), the prevailing clinical assessment of kidney function, suggesting PTs are an early target in cirrhosis that may not be captured by glomerular markers. Contrasting with passive filtration, the tubules depend on kidney cellular energy production for solute secretion and reabsorption. Various pathways have linked cirrhosis to impaired tubular metabolism including mismatched demands for sodium/water reabsorption, exposure to retained bile acids and toxins, and pro-inflammatory gut bacterial products, however further investigation of these early mechanisms is challenged by a lack of measures aligned with the target of injury or studies in patients with cirrhosis already experiencing overt kidney disease. I hypothesize that the collective ischemic and toxic-metabolic environment causes attenuation in kidney cellular metabolism, affecting downstream energy-dependent functions of tubular secretory clearance (TSC) and reabsorption, that is not captured by glomerular markers alone. I propose a prospective nested cohort study of patients with cirrhosis characterized with longitudinal data and biosample collections, multi- modal imaging, and gene expression profiling, to reveal novel pathways of kidney dysfunction and potential therapeutic targets, as well as more holistic assessments of kidney function beyond GFR. I will recruit 140 patients with cirrhosis and preserved eGFR to participate in 3 study visits to determine the association of baseline measures of PT function and injury with kidney-related outcomes (eGFR slope, acute kidney injury [AKI], and ascites severity). I will apply novel methods developed in our lab to estimate TSC by measuring plasma and urine levels of highly secreted endogenous solutes, which I have used in studies of AKI, drug clearance models, and CKD development. In a sub-cohort (N=20) compared to age-matched controls (N=20), I will delineate the effect of cirrhosis on tubular oxidative metabolism using state-of-the-art imaging with 11C- acetate as well as measuring TSC using an exogenous tracer, 99mTc-MAG3. Finally, I will obtain kidney biopsies in a sub-cohort (N=9) of patients with cirrhosis to characterize tubular pathways of injury, metabolism, and fibrosis using a novel spatial transcriptomics platform. As part of this career development award, this work will allow me to develop new expertise in study design, systems biology, and biostatistics, yield a novel cohort and data in patients with cirrhosis to uncover new insights into mechanisms of kidney dysfunction, and provides a basis for future discovery to develop monitoring and treatment strategies as an independent translational researcher of kidney dysfunction in cirrhosis.

NIH Research Projects · FY 2026 · 2026-03

The overarching objective of this project is to develop computational methods to infer cellular history from single-cell sequencing data, enabling insights into disease progression in tissues that are not longitudinally accessible, such as the brain to study Alzheimer’s disease or the heart to study cardiomyopathy. Current single-cell approaches excel at capturing static snapshots of cellular states but fall short in reconstructing earlier unobserved cell states and dynamic histories critical for understanding disease mechanisms. To address these gaps, this project proposes a three-pronged approach: 1) leveraging lineage-tracing single-cell RNA sequencing to quantify how far back cellular history can be inferred; 2) using single-cell RNA sequencing data from large donor cohorts to decode human-specific disease dynamics while accounting for biological and environmental variability; and 3) integrating single-cell multi-omics (e.g., RNA and ATAC-seq) to model regulatory mechanisms that drive cellular transitions over time. Each aim will be validated using systems where longitudinal sequencing is possible to ensure methodological rigor and biological relevance. By building upon cutting-edge statistical and artificial intelligence ideas, this research will uncover hidden cellular histories not observable in the collected tissue and identify critical early events in disease progression. These insights will advance fundamental knowledge of complex biological processes, inform therapeutic strategies, and align with the mission of NIGMS to enhance health and reduce disease burden by supporting innovative and impactful biomedical research.

NIH Research Projects · FY 2026 · 2026-03

Project Abstract This eMERGE IV (E4) supplement proposes extend the outcomes timeline for the prior implementation of 10 “genomic risk assessment” (GIRA) scores in a network-wide set of participants. These GIRAs include polygenic risk score (PRS) information, as well as risk information, such as personal and family health history, environmental and social health determinants, and physical and lab measures. Substantial challenges must be addressed before genomic medicine is a part of standard medical care. The specific aims of our proposal are designed to use an implementation science approach to advance the integration of genomic data into clinical practice, including evaluation of patient perspectives and economic outcomes, and broadening the impact of eMERGE through collaborations. The University of Washington Medicine dedication to preventative health in a learning health system and broad expertise across genomics, statistical, ethical, informatic, implementation, outcomes and economic disciplines will support this multi-site clinical trial. We will continue our leadership in data-cleaning and in the analyses of 6 and 12 month post-return outcomes data.

NIH Research Projects · FY 2026 · 2026-02

Influenza virus neuraminidase (NA) plays a central role in enabling influenza virus infection, transmission, and propagation, yet structural variation among influenza subtypes and structure-function relationships for this major surface glycoprotein remain poorly characterized. NA is a sialidase that cleaves sialic acid from host glycoproteins and glycolipids and is crucial for mediating disaggregation of viral particles, facilitating their release from host cells following budding assembly, as well as enabling their migration through mucus and the glycocalyx barrier surrounding cells during transmission and infection. NA is the target for anti-influenza sialic acid analog drugs such as oseltamivir (i.e. Tamiflu). NA is also increasingly recognized as an important antigenic target for protective antibodies, including some that are broadly cross-reactive against diverse strains and subtypes. Recent studies have indicated that NA exhibits considerable variation in its organization among diverse strains, however, in comparison to the other major influenza surface protein, hemagglutinin (HA), relatively little is known about structural variation among strains and subtypes and how that impacts NA function and immune recognition. While structures are available for the isolated catalytic head domain assemblies, often in re-engineered, stabilized forms, little data is available for the complete membrane-displayed assembly, despite the fact that key modulatory activities have been attributed to the portions of NA, such as its stalk that tethers the catalytic head to the viral membrane. These important domains are commonly removed for structural and in vitro studies. Indeed, perhaps the most striking type of NA variation involves significant sequence and length variation in the stalk domain. Dramatic length shifts in the NA stalks have been documented in conjunction with growth in specific host species, e.g. avian vs human. Changes in the stalk have also been reported to modulate NA catalytic activity, virulence and antibody recognition. The stalk is thus a critical, if poorly understood, modulator of IAV phenotype. Here, we propose to use cryo-electron tomography (cryo-ET) and hydrogen/deuterium-exchange mass spectrometry (HDX-MS) to resolve the structure, dynamics, and flexibility of native, membrane-presented influenza NA and their matched soluble ectodomains from a contemporary and ancestral avian H5N1 strain. Our experiments will test the effect of membrane anchoring and naturally occurring stalk truncations that have been reported to modulate NA’s oligomeric stability, enzymatic activity, host specificity, and viral pathogenesis. In parallel to the structural analysis, an array of sialidase activity assays will be performed to connect structure and NA function. These studies will provide new insight into NA’s structural variation, its native organization on authentic biological membranes, and structural determinants of its essential viral function.

NIH Research Projects · FY 2026 · 2026-02

Cannabis use during pregnancy has increased substantially, in conjunction with widespread decriminalization/legalization, changing public perceptions about harm, and evidence of cannabis’s antiemetic properties. Prior outcomes research on prenatal cannabis exposure is narrow in scope, as these older studies included research participants with polysubstance use (e.g., tobacco, alcohol, illicit drugs). In addition, prior research likely underestimated potential risks specific to cannabis use during pregnancy because modern strains are 10x more potent than they were 40 years ago. In our currently funded research, cannabis use is measured prospectively during pregnancy using weekly reports validated with labels and urine-based assays. Infants receive a neonatal neurobehavioral exam and multi-modal imaging (functional magnetic resonance imaging, myelin imaging, diffusion tensor imaging, and structural MRI) under natural sleep at 2-4 weeks-of-age and extensive neuropsychological follow-up assessments at 6 and 18 months. We propose to broaden the impact of this work by collecting longitudinal MRI scans concurrently with the 6- and 18-month neuropsychological visits. By focusing on the first 18 months of life, we aim to characterize cannabis-induced brain changes and dysregulated growth trajectories at a time when rapid synaptogenesis, axonal growth, and myelination is unfolding. In addition, we will test the hypothesis that prenatal cannabis exposure is more detrimental to females than males. This program of research aims to clarify potential health risks, enabling the general public to make better-informed choices surrounding cannabis use during pregnancy.

NSF Awards · FY 2026 · 2026-02

The United States faces a narrowing window to reestablish leadership in future global networking technology standards - the foundational rules that determine how next-generation communications systems (5G/6G, cloud/edge, AI-driven network management, and critical Internet infrastructure) are built, secured, and deployed. While U.S. innovation remains unmatched, U.S. influence in international networking standards bodies such as International Telecommunications Union (ITU) and Third Generation Partnership Project (3GPP) has weakened. Peer competitors are actively conducting coordination and collaboration to shape standards to favor their industrial policies and intellectual-property portfolios. Without a cohesive national strategy, the United States risks diminished influence over the technical and security foundations of future global internet/communications ecosystem undermining economic competitiveness, technology innovation, and supply chain resilience. The proposed Workshop is aimed as a forum for achieving strategic alignment via an all-hands approach among academia, government and the private sector to potentially: 1. Strengthen U.S. presence and influence in standards to compete globally by reducing barriers to market entry; 2. Spur domestic innovation in key supporting industries (cloud, semiconductors, AI infrastructure, telecommunications) through stable, widely adopted standards and encourage greater private-sector R&D investment by providing clearer pathways for commercialization; 3. Incentivize broad, sustained U.S. participation from startups, subject matter experts (SMEs), academia, and open-source communities who currently lack resources but drive much of the innovation shaping next-generation networks; 4. Establish national standards coordination framework that synchronizes R&D priorities, spectrum policy, and procurement with standards development timelines; and 5. Protect and advance U.S. security and economic interests to support secure-by-design architectures, supply chain transparency, interoperability, and resilience. This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.