University Of Alabama At Birmingham

NSF Awards · FY 2026 · 2026-07

This project is to support student travel at the 2026 IEEE-EMBS International Conference on Body Sensor Networks (BSN 2026). BSN is the premier conference in the areas of wearable sensing, mobile health, and computational medicine. It will bring together leaders and experts in academia, industry, healthcare, and non-profit organizations to provide a cross-disciplinary, highly selective, and single-track forum for cutting-edge research related to devices and sensors, hardware and software systems, artificial intelligence, predictive models, and data analytics in the healthcare/medical domains. Student participants will have opportunities to receive professional support and career advice from internationally recognized experts. Travel support increases engagement with the research community and provides professionally significant opportunities to students who might otherwise not be able to attend the conference. This project aims to increase the accessibility of the scientific forum that is BSN 2026. By attending BSN 2026, students may explore their interests, interact and network with seasoned professionals, and identify the various career paths available within the broader community of health scientists and technologists. With this registration award offsetting the cost of attendance, students who would otherwise find attendance expenses prohibitive can obtain these benefits. BSN 2026 will focus on cutting-edge innovations in computational medicine, including applications of novel sensors and artificial intelligence. Increasing student engagement through the reduction of expenses, this award constitutes an investment in the future of the medical sensor and computational medicine research community; a community that is critical to the next generation of healthcare. 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 · 2026-06

Funds are requested to purchase a Beckman-Coulter Optima Analytical Ultracentrifuge (AUC) equipped with Rayleigh interference, multi-wavelength UV-Visible absorbance detection, and required accessories. The instrument will be contained within the new Biophysical Chemistry Characterization Core (BC3) at the University of Alabama in Birmingham (UAB). The new instrument will serve as a replacement to the now obsolete 29-year- old XL-I analytical ultracentrifuge. The Optima AUC is the only commercially available analytical ultracentrifuge and, as of 2017, replaces the Proteomelab XL-I AUC, which is no longer manufactured nor supported by Beckman-Coulter. The new Optima AUC will be the only analytical ultracentrifuge at UAB and in the state of Alabama. The new Optima AUC will advance the health-related goals of multiple NIH funded research projects supported by R00, R01, R35, and R37 grants across multiple National Institutes of Health including, NIGMS, NIAID, NIDCR, and NINDS. This includes principal investigators from UAB departments across both the School of Medicine and academic units including the Departments of Chemistry, Biochemistry and Molecular Genetics, Microbiology and the UAB Center for Integrative Structural Biology. Results from this instrument will impact NIH- funded research in cancer, viral genome delivery and packaging, neurodegenerative diseases, proteome maintenance, transcription, pre-mRNA splicing, spliceosome assembly and function, HIV-1 viral assembly, biofilm formation, and dental caries (tooth decay). UAB’s mission is to enrich society and improve health and well-being through transformational educational experiences, groundbreaking research, innovation and entrepreneurship, community engagement, and world-class patient care while serving our UAB, local and global communities. Acquisition of this instrument aligns with this mission as it will bring unique biophysical characterization capabilities to UAB and the southeast region. UAB is an NIH Comprehensive Cancer Center (CCC), Comprehensive Center for AIDS Research (CFAR), and is one of the top 25 US universities for NIH funding. We have a plan for enlisting new NIH funded researchers from a vast pool of projects at UAB with a likely need for AUC. Furthermore, as a teacher/scholar and NIH funded investigator the PI is committed to training the next generation of biophysical chemists in rigorous and careful analytical techniques, including analytical ultracentrifugation. With nineteen years of classroom experience, the PI employs the most modern pedagogical techniques to teach both physical and biophysical chemistry. With this expertise, we have developed a novel training plan for teaching AUC. This aligns with the UAB mission to improve health and well- being through transformational educational experiences and will impact the broader biophysical community by training the next generation of biophysical chemists and AUC practitioners. In sum, advancing these NIH funded projects contributes to UABs long-range biomedical research goals and will stimulate biomedical research at UAB.

NIH Research Projects · FY 2026 · 2026-06

1 Alzheimer’s disease (AD) is a progressive neurodegenerative disease affecting approximately 6.7 million 2 Americans aged 65 and older and projected to reach 13.8 million by 2060. Progress in the management and 3 treatment of AD is limited by lack of early diagnostics, which are critical to the development of effective 4 therapies. AD is currently described in three stages: preclinical, mild cognitive impairment (MCI), and 5 Alzheimer’s dementia. The difficulty lies in detecting the disease during the preclinical phase, when patients 6 show no clinical symptoms of cognitive impairment but there is underlying pathology. Currently, we are limited 7 to detecting the accumulation of amyloid plaques in the brain using expensive and invasive methods such as 8 Positron Emission Tomography and cerebrospinal fluid assessment via lumbar puncture. The goal of the 9 proposal is to quantify and validate two novel retinal biomarkers for early AD detection and monitoring of 10 disease progression known as the retinal mid-peripheral capillary free zones (CFZs) and putative retinal 11 gliosis. As an extension of the brain, the retina provides a potential non-invasive window for early detection of 12 AD. Our group has recently characterized and quantified a novel retinal vascular biomarker for early AD 13 detection known as the retinal mid-peripheral CFZs (periarteriole and perivenule CFZs) using Optical 14 Coherence Tomography Angiography (OCTA). We have also recently shown larger surface area of putative 15 retinal gliosis in preclinical AD patients compared to controls in vivo using en face Spectral Domain OCT (SD- 16 OCT), suggesting putative retinal gliosis as a novel biomarker of AD-related neuroinflammation in the retina. 17 Building on these prior results, our central hypothesis is that these two novel retinal biomarkers will change 18 over time and will be associated with changes in plasma ptau217, and perivascular space burden on magnetic 19 resonance imaging (MRI) in early AD. We will test our central hypothesis by completing the following aims: 20 AIM 1: Determine if the retinal mid-peripheral CFZs change with disease progression and predict 21 changes in MRI perivascular spaces in the centrum semiovale in cognitively unimpaired (CU) older 22 adults at high-risk for AD. We will collect baseline and longitudinal OCTA and MRI data in high- and low-risk 23 CU older adults. AIM 2A: Determine if the surface area of putative retinal gliosis changes with disease 24 progression and predicts changes in plasma ptau217 in preclinical AD. We will collect baseline and 25 longitudinal en face SD-OCT and plasma data in preclinical AD patients and controls. AIM 2B: Compare the 26 diagnostic utility of putative retinal gliosis to plasma inflammatory panel to distinguish between 27 preclinical AD and controls. We will use baseline putative retinal gliosis, plasma GFAP, and proinflammatory 28 cytokine data to develop an ROC curve and classification comparison plots to distinguish between preclinical 29 AD and controls. This project will provide novel information about the association between changes in retinal, 30 MRI, and plasma biomarkers for early AD detection, and monitoring of disease progression.

NIH Research Projects · FY 2026 · 2026-06

PROJECT SUMMARY: This application is for F30 support of Madeline Ragland during the remainder of her MD-PhD training. The scientific focus of Madeline’s proposal is to analyze the ways in which top-down processing changes with central vision loss. Macular degeneration (MD) is one of the leading causes of blindness in the United States and can lead to impairments in daily functions like reading, cooking, and driving. However, some patients are able to compensate for these impairments through increased use of their peripheral vision. At the moment, the field does not have a clear understanding of the brain changes that arise following central vision loss. However, previous task-based fMRI papers in patients with MD have suggested that one potential change that might occur is a strengthening of feedback signals to primary visual cortex (V1), from higher order brain regions involved in cognitive processing (also known as top-down feedback). Top-down influences on visual processing are important for analyzing visual scenes, attending to specific areas of visual space and filtering out task-unrelated information. Therefore, one hypothesis that could explain why certain patients with central vision loss have fewer deficits than others is due increased feedback signals from higher order brain regions to peripheral V1. However, there has not been a study to definitively test this hypothesis. This proposal seeks to understand the behavioral and neural changes that result from increased use of peripheral vision, specifically examining the changes in top-down processing. A simulated model of central vision loss will be used where participants will be trained on a novel perceptual learning task to improve visual processing of peripheral vision. This intervention is part of a clinical trial being run by Dr. Kristina Visscher and Dr. Aaron Seitz. Changes in top-down processing will be assessed using a previously defined psychophysical task and through analysis of functional connectivity patterns in a task-based fMRI study. The knowledge gained from this proposal will help the field gain a better understanding of plasticity in adulthood and will help guide recommendations for rehabilitative strategies for patients with macular degeneration. More broadly, understanding how top-down processing changes with experience can be applied to other neuropsychiatric disorders where feedback signals are dysregulated in order to further explore how these networks can be modulated for therapeutic benefit. Madeline’s long term career goal is to run an academic research lab to better understand mechanisms of plasticity in neuropsychiatric disorders. To accomplish this goal, this project has been designed to deepen her understanding of systems neuroscience and computational methods so she can translate this theoretical knowledge into clinical applications such as alternative therapeutic strategies. Under the mentorship of UAB MSTP, Neuroengineering Program and Dr. Kristina Visscher, Madeline will have the tools and support necessary to accomplish the goals outlined in this proposal.

NIH Research Projects · FY 2026 · 2026-06

SUMMARY Epithelial morphogenesis involves cell shape changes, cell rearrangements, and spatially regulated cell division. It is a crucial process that is employed both during embryo development and in adult homeostasis. Dysregulated epithelial morphogenesis is associated with a range of human diseases, such as neural tube defects, highlighting the importance of this process. Despite this, our understanding of molecular control of epithelial remodeling is quite limited. In vitro cell culture models often do not capture epithelial morphogenesis in a precise and faithful manner. Hence usage of animal models is required to address detailed molecular mechanisms that regulate epithelial morphogenesis. In this project, we focus on a specific event during epithelial morphogenesis, namely apical constriction, a process whereby apical cell surface is actively reduced under the control of Rho signaling. We will investigate in depth an activator of Rho GTPases, the RhoGEF Plekhg5, in modulation of apical constriction. Our previous studies reveal that plekhg5 is necessary for apical constriction to make bottle-shaped cells during Xenopus gastrulation and sufficient to induce apical constriction ectopically in other epithelial cells. We further demonstrate that plekhg5 modulates dynamic apical actomyosin organization to reduce apical cell area, and it does so efficiently in part due to self-association of Plekhg5 protein to facilitate formation of a signaling platform. We plan to build upon these and other preliminary data to explore several additional hypotheses. In aim 1, we will test the hypothesis that apical constriction involves sequential events of junctional recruitment of Plekhg5, activation of Rho signaling, post-translational modification of Plekhg5, junctional release of modified Plekhg5, and translocation of Plekhg5 to the apical cortex to regulate actomyosin dynamics. In aim 2, we will examine the hypothesis that multiple regulators of actomyosin act downstream of Plekhg5 and activated Rho to regulate apical constriction of the bottle cells. In aim 3, we will investigate the hypothesis that human PLEKHG5 variants of uncertain significance can be studied in Xenopus to reveal differential effects of these variants on protein levels, localization, dimerization, activation of Rho, and/or interaction with other partners. Results from our studies will help uncover detailed mechanisms underlying the function of the RhoGEF gene plekhg5. The data will also provide deeper insight into general strategies that RhoGEF genes use to control biological processes during embryonic development. It will additionally present Xenopus as an attractive model to use for functional and mechanistic interrogation of human variants with uncertain significance.

NIH Research Projects · FY 2026 · 2026-06

Approximately 1/3 of patients with epilepsy are drug-resistant and should be considered for surgery. Successful epilepsy surgery depends on accurate localization of the seizure onset zone (SOZ), often requiring invasive monitoring with stereoelectroencephalography (sEEG). However, sEEG has inherent spatial limitations, and in many cases, imprecise localization contributes to surgical failure—observed in up to 60% of cases. EEG source localization (ESL) uses mathematical algorithms to localize seizure signals; this is an established technique for scalp EEG but has not been adapted to intracranial EEG. Our supporting data using corticocortical evoked potentials recorded from sEEG suggests that the distributed source algorithm SWARM may have less localization error and be less susceptible to the effects of sensor positioning and source location compared to other algorithms. However, seizure signals typically consist of low voltage high frequency activity, which presents different challenges for source localization and, thus, requires further validation before clinical application. The main goal of this project is to systematically examine the application of ESL techniques to sEEG- recorded seizures. The Specific Aims are: 1) Assess the accuracy and precision of sEEG source localization methods using stimulation-induced seizures.; and 2) Advance sEEG source localization as a predictor for seizure freedom following epilepsy surgery. This research will answer many important questions faced in applying these localization techniques to intracranial- recorded signals and will prepare for a larger prospective trial examining the value of sEEG localization in surgical decision making, utilization of sEEG-ESL for determining the extent of surgical resection, and comparison of sEEG-ESL with non-invasive scalp EEG-ESL and MEG. The applicant has dedicated his career as a clinician and researcher to improving the care of epilepsy patients undergoing surgery. To achieve this, he has begun his career as a tenure- earning Assistant Professor at the University of Alabama at Birmingham, where a supportive collaborative research environment in the Departments of Neurology, Neuroengineering, Neurosurgery, and Pediatric Neurology will make career advancement towards independence possible. To accomplish the goals of this research, the candidate has assembled a mentoring team with decades of experience in clinical trials, EEG/MEG source localization research, statistics, and faculty mentorship to advise and guide him during career development. He also proposes to take formal training in biostatistics, MEG and EEG signal analysis, and clinical trial design to complement his prior training with the skills necessary to transition to independence.

NIH Research Projects · FY 2026 · 2026-06

Byron Lai, PhD – R01 Project Summary/Abstract Children with physical disabilities face significantly higher risks for cardiovascular disease (CVD) and physical deconditioning as they age, primarily due to alarmingly low rates of exercise participation. Aerobic exercise is a proven non-pharmaceutical method for preventing CVD and maintaining health and fitness, yet common modalities like walking, running, and cycling are often inaccessible for children with mobility impairments. Disappointingly, children with disabilities often fail to engage in exercise at sufficient durations or health- enhancing intensities to elicit meaningful improvements in their health, particularly when the exercise is self- regulated and unsupervised by specialists. The rise of telehealth and widespread internet access offers a unique opportunity to deliver scalable, accessible, and age-appropriate exercise programs for underserved children with disabilities. This project aims to address this gap by conducting a 2-arm, parallel group, phase II randomized controlled trial (RCT) to evaluate the efficacy of a telehealth-delivered extended reality (XR) exergaming intervention on the health of children with cerebral palsy (CwCP). This innovative program leverages commercially available immersive gaming technology adapted for CwCP, behavioral tele-coaching, and caregiver involvement to help participants meet the recommended adult exercise guidelines of 150 minutes per week of moderate-intensity aerobic activity. The intervention is multi-level, targeting both the child and caregiver with behavioral strategies to enhance adherence. The intervention is based on our pilot work and integrates enjoyable, age-appropriate XR fitness games with adaptive gameplay to accommodate diverse levels of mobility and functional ability. The trial will enroll 130 physically inactive children with CP, aged 10–17 years, who will be randomized to either a 12-week XR exergaming intervention or a non-intervention control group. Outcomes will be assessed remotely using telehealth platforms and include measures of physical activity levels, cardiometabolic health indicators (e.g., blood pressure, cholesterol, hemoglobin A1c), and physical health and fitness (e.g., grip strength, cardiorespiratory capacity, functional mobility, and self-reported global health). A 24-week follow-up phase will evaluate the sustainability of both physical activity and health outcomes after the intervention, resulting in a 36-week study duration. If successful, this study will provide a transformative, scalable solution for increasing physical activity and improving health outcomes in children with disabilities, demonstrating the feasibility of meeting established exercise guidelines and building a robust foundation for understanding their effects on health in this underserved population.

NIH Research Projects · FY 2026 · 2026-06

PROJECT SUMMARY Survival of pediatric (age <18 years) out-of-hospital cardiac arrest (OHCA) depends on bystander cardiopulmonary resuscitation (CPR) administered by layperson community members until the arrival of emergency medical services (EMS) personnel. Unfortunately, CPR participation rates vary widely across the U.S. and are particularly low in Alabama, contributing to one of the nation’s lowest OHCA survival rates. Telecommunicator CPR (T-CPR) protocols, in which 9-1-1 call takers partner with the caller to identify an individual experiencing OHCA and provide real-time CPR instructions, may help improve recognition of pediatric OHCA and CPR delivery. However, no protocol has been developed and tested in populations of the Deep South. Our central hypothesis is that a tailored version of the commonly used ‘No, No, Go!’ T-CPR protocol for pediatric OHCA, co-adapted by community members and EMS stakeholders in Birmingham, Alabama, will result in high-quality CPR delivery and high participant satisfaction. We will test our hypothesis through the following specific aims: In Aim 1, we will evaluate the 'No, No, Go!' T-CPR protocol for pediatric OHCA through high-fidelity simulated OHCA sessions conducted with Birmingham community members residing in high-risk OHCA neighborhoods. We will assess implementation outcomes including feasibility, fidelity, acceptability, and appropriateness. Following the simulations, focus groups with participants will be conducted to gather feedback on the protocol and generate recommendations for improvement. In Aim 2, we will co-adapt the pediatric 'No, No, Go!' T-CPR protocol evaluated in Aim 1 in collaboration with community members and EMS stakeholders. We will then pilot a novel prototype T-CPR protocol designed to improve the effectiveness of bystander CPR delivery for pediatric OHCA by lay rescuers. This work builds upon Dr. Coute’s prior findings from his NHLBI K23 award and American Heart Association Early Independence Award focused on adult OHCA and will provide critical preliminary data to support a future R-level implementation trial.

NIH Research Projects · FY 2026 · 2026-06

Remote symptom monitoring (RSM) using electronic patient-reported outcomes (ePROs) during active cancer treatment improves symptom control, quality of life, time on treatment, and hospitalization rates in clinical trials and real-world settings. This prompted the Centers for Medicare and Medicaid Services (CMS) to mandate RSM use in their national value-based care initiative and to recommend implementation nationwide. To support this effort, the Patient-Centered Outcomes Research Institute (PCORI) funded the OncoPRO Initiative (DI-2023C1-31283) to expand RSM to 15+ health systems, guide implementation through a structured learning collaborative, and develop a generalizable toolkit to support future adopters. However, OncoPRO does not currently address how differences across sites, such as in patient populations served, infrastructure, and resource availability, influence RSM implementation and impact. This is a missed opportunity to generate insights that can guide more tailored strategies and support more efficient, effective scale-up. Early evidence shows wide variation in engagement, reporting, and barriers across settings, creating inconsistent outcomes and underscoring the need for context-sensitive guidance. This proposal leverages the national OncoPRO dataset to identify site- and patient-level variation in engagement, barrier experience, and implementation strategy use, and translate that knowledge into actionable guidance for novice clinical teams. In Aim 1, we will use latent class analysis and geospatial methods to derive patient engagement profiles and assess their geographic and contextual distribution. In Aim 2, we will use methods from cognitive anthropology (cultural consensus and residual agreement analysis) to model site-level variation in barriers and strategies and assess their relationship to implementation outcomes such as reach, adoption, and effectiveness. These findings will be used to develop an excel-based Precision Implementation Module (PIM) in Aim 3, consisting of a Practice- Context Mapping Tool and a Barrier Forecast and Strategy Menu that will support more tailored, site-led implementation planning using information that teams already know or can easily obtain. We will then refine the PIM through iterative interviews and focus groups with OncoPRO participants and prospectively pilot test it with 3-5 novice OncoPRO sites to evaluate its feasibility, acceptability, and appropriateness. This project builds on my foundation in anthropology and qualitative methods while supporting new training in large database analysis, implementation science, and pragmatic trial design. It will generate a scalable, context-sensitive resource to support tailored RSM implementation and lay the foundation for a future R01 evaluating the added value of precision implementation to traditional facilitation. This award will launch a rigorous, stakeholder- informed research program focused on improving how innovations are adapted and delivered across diverse cancer care settings. By bridging real-world needs with methodological precision, this work will help ensure that interventions like RSM are not only effective but feasible and impactful wherever patients receive care.

NIH Research Projects · FY 2026 · 2026-05

ABSTRACT: Sepsis is a heterogeneous syndrome consisting of overlapping phenotypes that cause a broad range of organ injuries. Sepsis-associated acute kidney injury (SA-AKI) is among the most consequential, with high mortality and poor functional outcomes. No direct disease-modifying therapies currently exist. A major barrier to therapeutic progress is the diversity of sepsis phenotypes, which leads to heterogeneity of treatment effect. A prominent, yet understudied SA-AKI phenotype involves viral priming preceding bacterial sepsis. First recognized in pediatrics due to the high prevalence of viral infections, interest in this phenotype grew during the COVID-19 pandemic. Viral-primed SA-AKI is marked by thrombotic microangiopathy, impaired renal microperfusion, and injury to renal tubular epithelial cells. Firmly rooted in this proposed pathophysiology is the interaction between renal endothelial cells and tubular epithelial cells. The objectives of this study are to understand the renal endothelial cell response to a synthetic analog of viral double-stranded RNA, polyinosinic- polycytidylic (poly(I:C)) acid, and to determine whether poly(I:C) mediated renal endothelial cell activation directly leads to downstream tubular epithelial injury. Preliminary data suggests poly(I:C) induces renal endothelial cells to produce type 1 interferons, which act in a paracrine manner to alert nearby cells to the presence of a viral infection. In isolation, poly(I:C) does not cause kidney injury. However, when poly(I:C) is given prior to low-dose lipopolysaccharide (LPS), a significant and disproportionate systemic inflammatory response with early, severe SA-AKI ensues. Together, these data support the novel hypothesis that systemic exposure to viral dsRNA activates renal endothelial cells and initiates a type 1 IFN response, thereby priming the kidney for exaggerated injury following a secondary bacterial challenge. To test this hypothesis, we will leverage in vitro and in vivo techniques to accomplish two specific aims. AIM 1 will focus on the renal endothelial cell response to poly(I:C) with and without LPS to establish type 1 IFNs as essential mediators in the development of viral primed SA-AKI. AIM 2 will examine the heterogeneity of viral responses among renal endothelial cell subpopulations using CITEseq, and will computationally define microenvironmental signaling networks between endothelial cells and renal tubular epithelial cells using single-cell RNA sequencing of whole kidney. This research training program will expand upon the candidate’s translational science background elucidating the role of chemokines involved in murine models of SA-AKI to gain new expertise in kidney physiology and vascular endothelial biology. The candidate will hone skills in cell culture, flow cytometry, single-cell RNA sequencing analysis, and laboratory management. Altogether, this career development award will facilitate the successful transition to scientific independence and the establishment of a reputable SA-AKI translational research program.

NIH Research Projects · FY 2026 · 2026-05

PROJECT SUMMARY/ABSTRACT This 5-year K01 proposal supports Seung-Yup “Joshua” Lee, PhD, in developing an independent research program to improve diabetes outcomes through AI-supported interventions targeting high-risk care transitions. Patients with type 2 diabetes (T2D) often manage complex medication regimens (e.g., insulins and GLP-1 receptor agonists), and medication changes during transitions from hospital to home create critical vulnerability in diabetes care. Despite medication reconciliation efforts, unresolved medication discrepancies across providers remain a major barrier to glycemic control, particularly among socioeconomically disadvantaged populations. Communication gaps between inpatient and outpatient providers further compound these challenges. Current healthcare systems lack effective, data-driven tools to identify and support high-risk patients following hospital discharge. To address this gap, Dr. Lee received a Forge AHEAD Center Pilot Award (funded through an NIH research initiative) to descriptively examine medication variability across care transitions and its association with HbA1c elevation (......), diabetes-related emergency department visits, and hospitalizations using retrospective electronic health record (EHR) data. This proposed K01 will support the development of MEDBRIDGE (MEDication BRIDGE at care transition), an AI-driven risk stratification tool to identify patients at elevated risk of adverse diabetes outcomes by integrating medication data (e.g., insulin types, GLP-1 receptor agonists, and medication changes at discharge), clinical factors (e.g., HbA1c and comorbidities), and social determinants of health (e.g., area-level composite indices, insurance status, and self-reported social history). It will also support pilot feasibility testing of a tailored intervention delivered by a nurse case manager (NCM) and community health worker (CHW), informed by MEDBRIDGE risk predictions. The study includes three Specific Aims: Aim 1: Develop, assess, and improve MEDBRIDGE models. Aim 2: Co-design a MEDBRIDGE-supported NCM/CHWdelivered intervention and train NCM/CHW. Aim 3: Pilot test feasibility, acceptability, and fidelity of the intervention post-discharge in a single-arm study. Dr. Lee’s training objectives are to 1) gain knowledge and expertise in diabetes medication management and discrepancy analysis; 2) develop skills and experience in qualitative and mixed methods research approaches; 3) build capacity in intervention design and pilot trial implementation; 4) advance professional development and progress to research independence. This 5-year K01 award will provide Dr. Lee with the mentorship, training, and research experience needed to become a leader in AI-supported patient-centered diabetes care. By the end of the award period, Dr. Lee will have generated novel data on reducing disparities in T2D outcomes and submitted a competitive R01 to evaluate scalable, datainformed interventions that improve glycemic control and reduce acute care utilization in high-risk populations.

NIH Research Projects · FY 2026 · 2026-05

Project Summary/Abstract Syphilis is caused by Treponema pallidum (T. pallidum) that can efficiently cross the placenta during all stages of pregnancy and cause fetal infection. In the absence of timely diagnosis and treatment in pregnancy, congenital syphilis (CS) can occur. CS rates have risen sharply in every region of the US over the past decade. Possible congenital syphilis is defined by in-utero exposure to syphilis in an asymptomatic infant with a negative syphilis evaluation (exam, CSF, CBC, and RPR ≤ 4-fold maternal RPR). Recommended treatment for possible CS is single dose benzathine penicillin G (BPG), an effective therapy that has intermittent shortages. The Congenital Syphilis Treatment Trial (CONSISTENT) was designed to test the efficacy of oral amoxicillin therapy (50 mg/kg po BID) compared to standard single dose intramuscular BPG therapy (50,000 u/kg) measured by serologic response within 6 months of treatment. CONSISTENT is a phase IV, open-label, randomized study that will enroll 374 infants (≥35 weeks) at twelve US clinical sites over a two-year enrollment period. Participants will be invited to participate in an optional pharmacokinetic substudy (n=30), and will have pre- and post-treatment oral/nasal swabs collected for T. pallidum PCR testing to carry out the following aims: Aim 1: Compare the treatment efficacy of liquid oral amoxicillin administered BID x 10 days compared to single dose IM BPG (standard of care) among 374 neonates with possible congenital syphilis; Aim 2: Confirm the oral amoxicillin dose of 50 mg/kg/dose BID for the treatment of congenital syphilis using the target plasma drug concentration of 0.42 mg/L as the MIC for T. pallidum; Aim 3: Assess the performance of quantitative PCR testing for T. pallidum on oropharyngeal and nasal swabs in refining the diagnosis of possible congenital syphilis in exposed neonates. Aim 1 will test the hypothesis that amoxicillin efficacy will be non-inferior (within a 10% margin) compared with standard IM BPG for the treatment of possible CS assessed by serologic RPR response within six months. Aim 2 will test the hypothesis that oral amoxicillin 50 mg/kg/dosed BID will be sufficient to maintain drug levels above the MIC threshold required to treat possible congenital syphilis. Aim 3 will test our hypothesis that newly developed quantitative PCR testing of easily collected oropharyngeal and nasal swabs will help refine and improve the diagnosis of syphilis in infants. Our expected outcome is to identify an alternative oral treatment option for infants with possible congenital syphilis. Our long-term goals are to improve options for the treatment and diagnosis of syphilis in infants to reduce long term adverse outcomes.

NIH Research Projects · FY 2026 · 2026-05

Abstract The development of advanced biomaterials capable of electrical signal transmission is vital for regenerative medicine and bioelectronics, with injectable conductive nanogels showing significant promise. While naturally occurring, biocompatible extracellular conductive nanowires (ECNs) from anaerobic bacteria, such as the multi- heme cytochrome proteins, offer a compelling solution to the limitations of synthetic materials (e.g., solubility and biocompatibility), their widespread application is currently limited by challenges in their rational engineering and efficient production. Specifically, the recently discovered ECN protein family has not yet been integrated into recent novel AI protein design tools, and their complex in vivo assembly mechanisms remain poorly understood. This proposal will bridge these gaps by first identifying and engineering OmcE cytochrome nanowires that form large, ordered bundles. This involves comprehensive large-scale genomic and AlphaFold3-guided virtual screens to pinpoint novel OmcE homologs, followed by high-resolution cryo-EM characterization to elucidate their structural details and bulk conductivity measurements to confirm electrical properties. Subsequently, state- of-the-art AI tools will be employed to engineer novel OmcE variants exhibiting robust self-assembly into advanced conductive nanogels. Simultaneously, another major objective is to visualize the OmcE secretion system in situ to unravel its intricate assembly mechanism. We hypothesize that these nanowires assemble via a large outer membrane porin, analogous to the chaperone-usher pathway. Sub-tomogram averaging will be utilized to reconstruct the porin's structure at sub-nanometer resolution, providing critical molecular blueprints for the rational design of OmcE variants with enhanced self-assembly properties and enabling their efficient recombinant overexpression. Ultimately, this work will facilitate the precise engineering of "super" OmcE nanowires for conductive nanogels, offering transformative insights into their biosynthesis and establishing a foundation for a new generation of protein-based bioelectronic materials.

NIH Research Projects · FY 2026 · 2026-05

PROJECT SUMMARY/ABSTRACT. Guidelines recommend measuring blood pressure (BP) outside of the office setting for diagnosing hypertension and managing BP. While out-of-office BP monitoring has generally focused on awake BP, over 50% of adults with hypertension have high sleep BP. High sleep BP is associated with increased risk for cardiovascular disease (CVD) events and kidney damage independent of office and awake BP. Therefore, obtaining both awake and sleep out-of-office BP measurements is important for identifying high out-of-office BP. Ambulatory BP Monitoring (ABPM) devices, which use an upper-arm brachial cuff worn for 24 hours, are the current reference standard for out-of-office awake and sleep BP measurement. ABPM is underutilized due to patient discomfort, lack of availability to clinicians, and high cost. Home BP monitoring (HBPM) devices can also measure BP outside of the office setting. Until recently, ABPM was the only device available to measure sleep BP. Newly developed brachial and wrist-worn HBPM devices offer a promising alternative to ABPM and can potentially overcome several barriers to ABPM use. However, similar to ABPM, brachial cuff HBPM disrupts sleep and is not well tolerated. Preliminary data suggest that wrist-worn HBPM devices cause less discomfort and are less likely to disrupt sleep compared to ABPM and brachial-cuff HBPM. Thus, a wrist-worn HBPM device that measures sleep and awake BP and disrupts sleep less than ABPM could replace ABPM for out-of-office-BP measurement if sleep and awake BP on wrist-worn HBPM have strong associations with end organ damage. There are few data on the association of awake and sleep BP obtained using wrist-worn HBPM devices with end organ damage. The goal of this study is to compare the associations of sleep and awake systolic BP (SBP) measured by wrist-worn HBPM versus ABPM with left ventricular mass index (LVMI) and albuminuria, validated markers of CVD and kidney damage. We hypothesize that the associations of sleep and awake SBP with LVMI and albuminuria will be stronger for wrist-worn HBPM than for ABPM. We will enroll 742 adults with office SBP of 110-159 mm Hg, including 50% on antihypertensive medication, from Birmingham, AL and New York, NY. Participants will undergo 24-hour ABPM and 7 days of wrist-worn HBPM in random order. LVMI will be assessed by echocardiography, and albuminuria will be measured from urine samples. The proposed study will determine if a novel wrist-worn HBPM device can be used as a clinically validated alternative to ABPM for diagnosing hypertension and managing BP. This study addresses NHLBI’s mission to optimize novel diagnostic strategies to prevent CVD.

NIH Research Projects · FY 2026 · 2026-05

PROJECT SUMMARY/ABSTRACT Restless legs syndrome (RLS) is prevalent and growing disease that causes a significant decrease in quality of life for many patients. These patients chronically suffer from a strong urge to move their leg that particularly worsens in the evening that is temporarily relieved by limb movement or getting up and moving around. This leads to a lack of sleep resulting in excessive daytime sleepiness, decreased work productivity, decreased quality of life and an increased risk of heart disease and stroke. Many continue to suffer despite standard of care medication use, often due to inadequate symptom control or intolerable, dose-limiting side effects of these neuroactive medications. These treatment resistant patients are left with few options for relief. Some will pursue long-term opioid treatment despite the stigma, regulatory difficulty, and potentially life-threatening side-effects. Investigation of alternative, non-medication, non-opoid options is crucially needed. Neuromodulation via spinal cord stimulation (SCS) was first reported as a successful therapeutic alternative for RLS in a patient with neuropathic pain by the primary investigator in 2016. Since then, there has been a growing number of reports corroborating this observation. However, these reports are limited to patients (with exception of one) with neuropathic pain and co-morbid RLS. To address this knowledge gap, rigorous study of SCS as a potential safe and effective novel therapy for treatment resistant, primary RLS is needed. Here we will utilize the collaborative expertise at UAB, international experts in RLS at John Hopkins and national experts in SCS at UCSF, along with our industry partner Saluda Medical (pioneer in adaptive/closed loop SCS) to perform a first-in-human controlled assessment of safety, patient acceptance, and preliminary effectiveness of SCS for primary, treatment resistant RLS. We will measure patient subjective, clinician subjective, and objective outcomes to assess for safety and improvement in RLS symptoms, sleep, and quality of life. Additionally, will use a combination of standard laboratory and novel home ambulatory measurements of sleep and leg movements. Furthermore, we will use a multimodal neurophysiology approach to test the spinal cord hypersensitivity pathophysiology theory of RLS. Our vision is to use this proven safe and effective neuromodulatory technique for neuropathic pain towards this novel indication to reduce human suffering while furthering our understanding of RLS pathophysiology and SCS mechanisms.

NIH Research Projects · FY 2026 · 2026-04

Abstract Cystic fibrosis (CF) is caused by a dysfunctional cystic fibrosis transmembrane conductance regulator (CFTR) protein, leading to impaired mucociliary clearance and the accumulation of thick mucus in the airway, often resulting in chronic bacterial infections. Bacteria within the Burkholderia cepacia complex (BCC) are associated with severe infections in people with CF (pwCF). BCC species are inherently antibiotic-resistant, making effective treatments for BCC infections scarce. One potential therapeutic target for BCC treatment is the pili that mediate virulence factors like adherence and biofilm formation. One type of chaperone usher pathway (CUP) pilus, known as "cable pilus," is often implicated in facilitating host adherence and drive biofilm formation in the BCC. However, it remains unknown whether the cable pilus is the sole pilus type produced during different stages of BCC infections, and no structures of BCC pili have been characterized. Currently, highly effective CFTR modulator therapies (HEMT) are commonly used in pwCF. However, the influence and interaction of BCC infection with host cells under HEMT remain unclear. This F31 proposal aims to elucidate the dynamics of BCC pili production and characterize the functions of these pili in CF infection. We hypothesize that multiple types of BCC pili are present and contribute differently at various stages of infection, including adherence, colonization, and biofilm formation. Aim 1 of this proposal explores the effect of different growth conditions on BCC pili production and the roles of pili in adherence to epithelial cells. We will utilize cryogenic-electron microscopy (cryo-EM) and adherence assays, and mutagenesis methods to characterize the pili produced by BCC and their role in adherence. Aim 2 investigates the interaction of BCC cells with CF epithelial cells in situ. We will use cryo-electron tomography (cryo-ET) to visualize interfaces of CF cells with BCC in the presence and absence of ETI HEMT.

NIH Research Projects · FY 2026 · 2026-04

Cannabis use is high in PLWH, ~25-35% of PLWH report cannabis consumption. Cannabinoids have been shown to have anti-inflammatory properties in humans and animal models. Heavy cannabis use in PLWH on ART is associated with decreased levels of activated T cells in peripheral blood. The two main cannabinoids present in cannabis are Δ9-tetrahydrocannabinol (THC) and cannabidiol (CBD). THC, the psychoactive component of cannabis, is a partial agonist for cannabinoid receptors CB1 and CB2. CB1 is primarily expressed in the brain while CB2 is reportedly expressed in immune cells, including CD4+ T cells. THC exposure modulates human CD4+ T cell gene expression and in animal models skews immune responses towards a Th2 phenotype and increases CD4+ T cell production of anti-inflammatory and immunosuppressive cytokines. CBD has anti-inflammatory and antioxidant effects without the psychoactive properties of THC. CBD exposure has been shown to suppress T cell proliferation, T cell production of IL-2 and IFN-γ production in T cells. Cannabinoid treatment has also been shown to suppress neuroinflammation in animal models of Alzheimer’s disease and multiple sclerosis. Importantly, in non-human primates (NHP) cannabinoid treatment reduced SIV-induced neuroinflammation. Based on these immunomodulatory properties of cannabinoids, we hypothesize that cannabinoids impact HIV infection and persistence in the CNS. Currently, it is not known how cannabis use impacts the phenotype of CD4+ T cells in the brain and their relative abundance and distribution. Therefore, as part of this project we will evaluate the effect of cannabinoids on the natural homeostasis of human T cells in the brain. We will then assess the impact of cannabinoids on the seeding of HIV infection in CD4+ T cells in the brain, the establishment of HIV latency in brain CD4+ T cells, and the efficacy of latency reversal agents to induce HIV expression in CD4+ T cells in the brain under ART-suppression.

NIH Research Projects · FY 2026 · 2026-04

Despite advances in our understanding of genetic basis of disease risk and advances in technology enabling genomic risk assessment, implementation of genomic medicine is limited. Many individuals at risk for common, actionable genetic conditions remain undiagnosed and most are unaware of their risk. Population genomic screening offers the opportunity to address these gaps by enabling early detection and intervention. Incorporating genomic screening into primary care could transform chronic disease prevention. To generate evidence on feasibility, clinical utility, and impact on health, working with our community stakeholders, we will develop and implement a pilot program for population genomic screening for common, actionable genetic conditions in primary care. In collaboration with the network, we will select conditions for which genomic screening can have a high-impact and strong evidence of preventing or mitigating disease severity. We propose screening for the three Centers for Disease Control and Prevention (CDC) Tier1 conditions (hereditary breast and ovarian cancer, Lynch syndrome, and familial hypercholesterolemia) and three additional conditions (Transthyretin amyloidosis, Hypertrophic cardiomyopathy, and APOL1 hypertensive renal disease) each chosen due to their particular significance in our patients and communities. We will engage stakeholders (PCPs, clinic staff participants, community members) to inform implementation and evaluation of genomic screening. We will develop a network-wide protocol to deploy the population genomic screening for the selected conditions in 5000 participants at our site (20,000 across the network). We will return results to the provider and participant and assess adoption of recommendations. Finally, we will evaluate participant outcomes over 24 months and examine the impact of the chosen implementation strategies on the adoption and integration of population genomic screening in primary care and share the implementation framework for population genomic screening in primary care. We bring together a team of national leaders with expertise in chronic disease genomics, clinical genetics, cancer genetics, cardiogenomics, implementation science, community engagement, and clinical informatics to translate genomic insights into clinical care. In collaboration with the community, clinical stakeholders, and the network, we will establish best practices for broader adoption of population genomic screening in primary care.

NIH Research Projects · FY 2026 · 2026-04

Abstract Respiratory viral infections (RVI) are a burden for society since they produce short- and long-term sequelae that impair the lung function. The impact of RVI is enhanced in newborns and young infants since their immune system is defective in generating protective CD8 T cell responses. Our published work in Science Immunology described a new form of XCR1+ dendritic cell maturation that impair the differentiation of IFNg effector cells in neonatal lungs. This form of regulatory cDC1 maturation (mregDC1) depends on the recognition of apoptotic cells and unlike proinflammatory cDC1, mregDC1 do not require TLR or microbiota for their maturation. In non- infected mice, the pulmonary mregDC1 is abundant during the first 14 days of life, suggesting that the increased susceptibility to RVIs in neonates is caused by mregDC1 differentiation (our central hypothesis). Due to their novelty, the role of mregDC1 in the neonatal immune responses against neonatal RVI has not been studied. To answer this question (Aim 1), we have generated two unique mouse strains with genetic deletions affecting only the cDC1 lineage and mregDC1 differentiation. Using these mice and in the context of Influenza A virus (IAV) infection, we will study whether mregDC1 protect the neonatal lung from inflammation at the expense of the ability to control IAV, whether T cells primed by mregDC1 are forced into a memory-like phenotype, and whether lacking mregDC1 during IAV infection carries a risk of breaking peripheral tolerance. Although the cDC1 lineage specializes in CD8 T cell activation, they can also present antigens in MHC-II molecules and interact with CD4 T cells. In aim 2.1 we will characterize the transcriptomic program induced in CD4 T cells by mregDC1, we expect to find a previously unknow way to induce anti-inflammatory functions in CD4 T cells. Finally, in mice and humans mregDCs have the capacity to induce changes in stromal cells. In mice mregDC1 alter the lymph node endothelial and fibroblastic reticular cells, while in human adults, mregDCs can induce the formation of tertiary lymphoid structures in the lungs. In aims 2.2 (mice) and 3 (human infants), we will perform spatial proteomic analysis of the mregDC1 – lung stromal cell interactions and study the structural changes to the lungs in the absence of mregDC1 (aim 2.2) or changes to mregDC1 development when alveolarization is interrupted (aim 3.1). Overall, our proposal will define the role of mregDC1 in promoting postnatal lung development while protecting the neonatal lungs from RVI and T cell mediated inflammation.

NIH Research Projects · FY 2026 · 2026-04

ABSTRACT Glaucoma is a leading cause of permanent vision loss worldwide, but the mechanisms of damage are still poorly understood. The only proven effective therapeutic intervention for glaucoma is intraocular pressure (IOP) reduction, although the “safe” IOP threshold varies widely among individuals. The preponderance of evidence suggests that the RGC axons are damaged in the laminar region of the optic nerve head (ONH) through which the retinal neurons transmit visual information to the brain. Individual susceptibility could be due to eye-specific factors such as ONH morphology and tissue compliance that modulate mechanical strain and blood perfusion in the neuroretinal rim and ONH. Hence, early diagnosis and screening is particularly challenging, and there is no accepted method for clinical assessment of eye-specific susceptibility to IOP. The goal of this project is to develop and validate mechanical, vascular and morphometric biomarkers of eye-specific susceptibility to glaucoma onset and progression. In this project, we will perform longitudinal optical coherence tomography (OCT) imaging procedures that quantify ONH mechanical deformations (strain) and vascular perfusion in vivo in response to precisely controlled acute IOP and cerebrospinal fluid pressure (CSFP) elevations, in an animal model of unilateral glaucoma instrumented with continuous IOP and CSFP telemetry. Data will be collected longitudinally, starting while the while the treated eye is normal and progressing through glaucoma onset and progression to endpoint. We will then use novel 3D histologic reconstruction techniques to quantify the full morphology of the ONH macroarchitecture and laminar load-bearing and neural tissue microarchitectures, and build and analyze eye-specific computational models of those tissues that are validated against in vivo, image- based strain measurements in those same eyes. We will then use artificial intelligence (AI) and geometric deep learning to determine the predictive relationships between longitudinal axon loss, visual function loss, differential IOP/CSFP in fellow eyes (mean values and their fluctuations), ONH and laminar tissue macro- and microarchitecture morphology, in vivo OCT-derived ONH strain and vascular perfusion, and computational estimates of strain in the laminar load-bearing and neural tissue microarchitectures. We will thus identify biomechanically relevant biomarkers that predict susceptibility to glaucoma onset and greater risk of glaucoma progression. Impact: This project will establish a link between clinically measurable ONH strain/morphology, perfusion, and eye-specific susceptibility to both glaucoma onset and progression that will underpin new diagnostic approaches. Results will identify critical biomechanics-relevant biomarkers of glaucoma onset and progression risk that can translate to patients, elucidate disease mechanisms and therapies targeted at altering ONH biomechanics.

NIH Research Projects · FY 2026 · 2026-04

We are at a watershed moment in human biology were we have identified that we have an axillary microbial genome that affects how our cells function and we can leverage this genome to tackle complex diseases such as diabetic retinopathy (DR). Thus, the human host is inextricably linked to its microbiome and has coevolved with it resulting in the outsourcing of approximately 60% of human metabolism to microbiota. The gut provides the dominant microbiome in the body, representing approximately a 3000 microbial species that are responsible for the generation of biologically active metabolites that dramatically impact host health. Microbiota-derived metabolites such as tryptophan (Trp) metabolites, short-chain fatty acids, and bile acid derivatives are crucial for gut health, beneficially influencing gut barrier function, immune responses, energy metabolism and lipid digestion. We have identified specific beneficial microbe derived metabolites of Trp that are decreased and other deleterious metabolites that are increased in the plasma of diabetic individuals with retinopathy. Using liquid chromatography–mass spectrometry (LC-MS) for targeted metabolomics, we show that individuals with DR have markedly reduced levels of the protective Trp metabolite, indole 3- proprionic acid (IPA) and elevated levels of toxic metabolite Indole sulfate. Exogenous administration IPA prevented the development of DR in db/db mice, a model of type 2 diabetes. IPA administration activated pregnane X receptor (PXR) receptors to enhance intestinal and retinal barrier function. IPA suppressed NF-κB signaling and NLRP-3 activation and downregulated pro-inflammatory cytokines such as IL-6 and TNF-α in the retina and reduced Th17 cells migration from the gut to the retina. We propose the following hypothesis: Key beneficial microbial derived metabolites such as IPA generated by the gut microbes enter the systemic circulation and retina activating PXR receptors on retinal endothelial cells and retinal pigment epithelial cells to main integrity of blood retinal barrier and modulate local retinal immune responses. These protective mechanisms are lost in DR. We postulate that Trp supplementation in the form of Trp containing dipeptides and/or genetically modified bacteria that generate beneficial Trp metabolites will prevent DR. Impact: nutraceutical supplementation with Trp or Trp containing dipeptides or intake of food grade probiotics that generate beneficial bacterial metabolites represent novel strategies for prevention of DR and are timely approaches for this era of personalized medicine.

NIH Research Projects · FY 2026 · 2026-04

This Type 1 hybrid effectiveness-implementation randomized controlled trial, Remote Fentanyl Test Strip Distribution and Education to Prevent Drug Overdose, aims to address the United States opioid crisis driven by fentanyl and other synthetic opioids. Fentanyl test strips (FTS) are a cheap, low burden tool used to detect the presence of fentanyl in drugs, and they are associated with high acceptability, yet critical FTS knowledge and implementation gaps persist. Moreover, extant studies of FTS programs are either limited to one city or region and enroll from brick-and-mortar sites, with no remote randomized controlled trials (RCTs) to date. Our study would be the first national, fully remote RCT to assess the impact of FTS on overdose outcomes among people using illicit stimulants and/or opioids. This project adapts our Remote Opioid Overdose Education and Naloxone Distribution intervention to FTS using a human-centered design approach, leveraging partnerships with national and regional community partners to co-create a fully remote intervention. We will use a 2x2 design to cross remote FTS distribution with remote FTS education, thereby isolating the individual and combined effects of the two components. The R61 phase focuses on adapting and piloting the interventions with 100 participants, assessing feasibility, acceptability, and appropriateness. The R33 phase implements a fully powered trial to compare overdose outcomes (fatal and non-fatal) among 2,952 participants randomized to the four study arms, which include: FTS distribution and education, FTS education only, FTS distribution only, and a control group. All groups will receive a resource list for naloxone and FTS. The secondary outcome is FTS knowledge, while exploratory outcomes include behavioral strategies to reduce risk of overdose (including FTS-specific behaviors) and utilization of substance use services engagement and treatment. The study also incorporates ecological momentary assessment to offer insights into daily contextual factors influencing FTS use, as well as a cost-effectiveness analysis to determine the most cost-effective approach with most overdoses averted. The study’s 2x2 design allows for a thorough examination of the interactions between FTS distribution and education, identifying the most effective and cost-efficient approach for reducing overdose rates. Overall, findings will inform the scalability of remote overdose prevention interventions. This work represents a sustainable, fully remote model that can be implemented nationwide, setting the stage for transformative advancements in overdose prevention.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY This hypothesis-driven, patient-oriented pilot randomized clinical trial will evaluate whether providing a high- energy human milk diet during the first two weeks after birth reduces respiratory morbidity in extremely preterm (EPT) infants. EPT infants, born at 28 weeks of gestation or earlier, have immature lungs and a high risk of developing bronchopulmonary dysplasia (BPD)—a chronic lung disease that increases mortality and long-term developmental complications. Early enteral nutrition is critical for lung development, yet most EPT infants receive insufficient energy during the first 14 days after birth. Docosahexaenoic acid (DHA) and arachidonic acid (ARA) supplementation is a promising strategy to increase energy intake through human milk, but there is no consensus on whether fat- enriched or protein-enriched diets are more beneficial for improving lung function. Building on findings from our recent NIH-funded trial, which demonstrated that protein-enriched diets improved growth and potentially reduced BPD severity, we will now assess whether a DHA/ARA-enriched exclusive human milk diet can achieve superior benefits. In this trial, we will randomize 150 EPT infants to receive either an exclusive human milk diet enriched with a commercially available DHA/ARA supplement or a standard, exclusive human milk diet during the first 14 days after birth. The primary outcome is the severity of respiratory morbidity at term equivalent age. We will also evaluate the feasibility of using non-invasive oscillometry to measure lung function in this population. This study will inform the design of a larger clinical trial and may establish that early enteral energy provision— unlike parenteral nutrition—provides measurable respiratory benefits. The findings could reshape neonatal nutrition strategies and optimize care for preterm infants at risk of BPD.

NIH Research Projects · FY 2026 · 2026-04

PROJECT SUMMARY/ABSTRACT Kidney disease contributes greatly to the elevated morbidity and mortality of women with systemic lupus erythematosus (SLE), a systemic autoimmune disorder. The problem of kidney disease is twofold. It is not only a direct health burden but also contributes to the progression of hypertension and cardiovascular disease (CVD), which is the leading cause of death in SLE patients. Over 50% of SLE patients have lupus nephritis, a specific kidney disease of SLE, and roughly half of SLE patients have hypertension. Therapeutic regimens for SLE often cause further kidney injury and worsen hypertension, which is already poorly controlled in this population. Because kidney disease contributes directly to patient morbidity and mortality and also worsens the development of hypertension and CVD, a better understanding of the pathological processes at work within the kidneys is necessary. Circulating autoimmune cells have been the focus of many basic and clinical studies, but the role of kidney resident memory T cells (TRMs) and inflammation within the kidney remains poorly understood. Thus, the central goal of this proposal is to identify the contributions of TRMs to kidney inflammation and hypertension in order to improve future care for SLE patients. Past research has broadly focused on CD4+ vs CD8+ T cell distinctions and various circulating cytokines as causal factors in SLE, but studies investigating the role of TRMs in the pathology of SLE-associated inflammation and hypertension are lacking. TRMs by nature exist entirely within a tissue through adhesion to epithelial cells like kidney tubular cells, which TRMs then target with lytic granules and other pro-inflammatory cytokines, causing kidney inflammation. Thus, in this proposal, specific aim 1 will test the hypothesis that TRMs directly mediate glomerular inflammation and injury in SLE through pro-inflammatory cytokine production. Recent research in the DOCA-salt model of hypertension highlighted CD8+ T cells' ability to upregulate tubular sodium transporters and mediate hypertension. Because similar mechanisms may be at work in SLE, Specific aim 2 will test the hypothesis that kidney TRMs mediate SLE-associated hypertension by augmenting renal tubular sodium reabsorption. Specific aim 3 will test the hypothesis that renal tubule derived molecules, namely CD155, IL-15, and TGF-β stimulate kidney TRM differentiation and activation in SLE. Dr. Moore will receive new training in techniques including T cell co-culturing with kidney cells and blood pressure radiotelemetry implantation and analysis and will gain additional experience in immunological and kidney injury analyses in the NZBWF1 female mouse model of SLE. The experiments and goals of this proposal will shed light on the mechanisms by which TRMs mediate kidney inflammation and hypertension in SLE and will provide Dr. Moore with the professional development, technical experience, and key hypothesis-generating data he will need to transition into an independent academic scientist investigating the contributions of the immune system to cardiovascular and kidney disease.

NSF Awards · FY 2026 · 2026-03

The University of Alabama at Birmingham (UAB) will host the 59th Annual Spring Topology and Dynamical Systems Conference (STDC), March 11-13, 2026, in Birmingham, Alabama. The STDC is one of the longest standing regular conferences in general topology, having started in 1967 and continuing as an annual conference. It attracts participants nationally and internationally. There are 7 plenary talks and 12 semi-plenary talks in most areas of topology and its applications by established researchers. Talks bridging two or more research areas are encouraged. In a highly technological society like the USA, a high level science research, and in particular mathematics research, is crucial for further progress. Conferences are an essential part for developing successful and competitive research programs in mathematics and for the education of young researchers. The STDC has played an essential part in the success and education of many of its participants. The conference will include contributed talks by PhD students, post-doctoral students, as well as junior mathematicians. There are six special sessions in subareas of topology including a new session in Applied Topology and Topological Data. The 59th Spring Topology and Dynamical Systems Conference will run six special sessions: Continuum Theory, Dynamical Systems, Geometric Topology, Geometric Group Theory, General and Set Theoretic Topology, and Applied Topology and Topological Data that will include most topics of contemporary research in topology as well as highlighting connections between topology and other mathematical subjects. The winner of the Mary Ellen Rudin Award for beginning mathematician will be announced at this meeting and will be invited to give a plenary address. The conference has succeeded in strengthening major connections between areas which normally do not interact. Particularly effective have been interactions between dynamical systems and continuum theory, between geometric topology and continuum theory, between geometric topology and geometric group theory, and between set theoretic topology and continuum theory. The interaction between these areas and graph theory is being encouraged by particularly inviting speakers who can bridge between the former areas and graph theory. The STDC encourages these interactions by providing travel support to students, post-docs, and junior mathematicians. More information and an invitation to participate may be found at the conference website: https://scholarlattice.org/collections/ddc12896-b56a-4419-872b-1a0a0a161829. 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.