University Of South Florida

NSF Awards · FY 2025 · 2025-06

Hands-on training helps students bridge theoretical knowledge with practical application in cybersecurity. While remote platforms offer excellent opportunities for learning software security, no comparable resources exist for hardware security education. Key topics in hardware security require access to physical development boards, creating a significant barrier for learners without these resources. In this interdisciplinary project, a remote platform will be designed to provide open access to physical hardware for beginners to advanced-level hardware security experiments. By providing a scalable, accessible, and innovative educational resource, this tool will advance hardware security education, support the development of skilled practitioners in this field, and respond to national security needs. The remote platform will consist of an array of hardware security development boards, comprising microcontrollers, Field Programmable Gate Arrays (FPGAs), built-in power side-channel measurement and fault injection hardware. The software will include a user-friendly front-end based on JupyterLab and an open-source backend for C and FPGA development. The project will also develop extensions for collecting important educational benchmarks and usage statistics, enabling the evaluation of pedagogical strategies for remote hardware labs. Students will design and conduct complex hardware security experiments on remote physical boards using Python to control the hardware and analyze outputs. By combining innovative hardware tools with scalable software solutions, the platform will enhance both the accessibility and effectiveness of hardware security education and foster advancements with teaching and learning in the field. This project is supported by the Secure and Trustworthy Cyberspace (SaTC) program, which funds proposals that address cybersecurity and privacy, and in this case, cybersecurity education. The SaTC program aligns with the Federal Cybersecurity Research and Development Strategic Plan and the National Privacy Research Strategy to protect and preserve the growing social and economic benefits of cyber systems while ensuring security and privacy. 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 · 2025-06

PROJECT SUMMARY The emergence of resistance to frontline therapies in the malaria parasite underscores the pressing need for sustained drug discovery and development efforts. Protein translation is largely unexplored in malaria parasites, yet recent studies highlight the translation machinery as a promising target for novel antimalarial drugs. Our work on the DDX6-family RNA helicase DOZI has uncovered that the human malaria parasite Plasmodium falciparum utilizes different membrane-less cytoplasmic messenger ribonucleoprotein (mRNP) granules to control protein translation. These granules, akin to processing bodies, stress granules, and germ cell granules in model eukaryotes, orchestrate various mRNA metabolism functions, encompassing RNA decay, storage, and translation repression. Building upon these findings, we posit that distinct mRNP types play pivotal roles in global and transcript-specific mRNA regulation, governing parasite development, life stage transitions, and survival under stress. To elucidate these regulatory mechanisms, we employ cutting-edge techniques in reverse genetics, protein biochemistry, microscopy, transcriptomics, and proteomics. Our first objective is to identify molecular markers for distinct mRNPs, determine their protein and mRNA compositions, and characterize their dynamics across different parasite life stages and under stress conditions. Secondly, we will delve into the functions of key RNA-binding proteins within the mRNP granules, deciphering their roles in regulating mRNA stability, decay, and translatability. While these aims are sufficiently independent to be carried out in parallel, their intermediate results will mutually inform and reinforce one another, augmenting the overall significance and feasibility of the study. Collectively, the insights gained from these objectives will contribute to a comprehensive understanding of the diverse roles of mRNPs in regulating critical aspects of P. falciparum biology, laying the groundwork for discovering new antimalarial drugs.

NIH Research Projects · FY 2026 · 2025-06

Project Summary/Abstract SARS-CoV-2 has been associated with neurological symptoms, although there is no strong evidence of a direct viral infection in the brain. Recent reports indicate that SARS-CoV-2-induced systemic inflammation and the cleaved S1 subunit of the S protein remain detectable in patients with COVID-19 for months after diagnosis and may cause neurological manifestations. Also, COVID-19 tends to be more severe in older people, and although various biological responses change with aging, the induction of cellular senescence (SC) is predominant. New findings indicate that SARS-CoV-2 induces senescence in the lung epithelium with an exacerbated senescence- associated secretory phenotype (SASP) in response to the S1 subunit of the SARS-CoV-2 spike protein. Here, we will investigate how SARS-CoV-2 promotes CS in the brain and the role of SASP components in conveying senescence and promoting AD pathogenesis. Our preliminary data show that the S1 protein enters the systemic circulation and accumulates in the choroid plexus (CP) epithelium that expresses the ACE2 receptor. When S1 is combined with systemic inflammation, it induces a senescence-like phenotype in the brain of aged mice, initially restricted to epithelial cells in the CP, but it spreads to other brain regions, including the cortex and hippocampus, within a month. Transcriptome analysis in the brains of aged S1-challenged mice with systemic inflammation 30 days post S1 administration identified the "metabolic pathways," "pathways in neurodegeneration," and "Alzheimer's disease" among the top 10 enriched pathways. We also investigated how the S1 cleaved subunit induces cellular senescence (CS) in the choroid plexus epithelial cells when combined with systemic inflammation, and our results indicate that S1 induces dysfunction of the Nrf2-antioxidant response, which leads to accelerated CS when it is accompanied by LPS-induced ROS production. Most importantly, SASP analysis revealed the role of soluble factors SASP and EV-miRNA SASP components in conveying CS of neurons and regulating CS and AD pathways, respectively. Therefore, our goal is to explore whether miRNA replacement therapy can abrogate secondary SASP-induced senescence and AD pathogenesis and progression. Furthermore, analysis of postmortem brain sections and CSF from AD patients revealed the presence of CS markers in the CP long before the robust accumulation of β-amyloid and tau tangles in HPC, suggesting that CS may play an important role in Alzheimer's pathogenesis. Analysis of CSF from the early stages of AD also showed high levels of soluble SASP factors, which correlates well with the cellular senescent burden in the CP that produces the CSF. These findings prompted us to examine the relationship between CS and SARS-CoV-2 infection further and how it may increase the risk for AD. Our hypothesis is that SARS-CoV- 2-induced SASP in the CSF induces neuronal senescence and increases AD risk. Patients with severe COVID- 19 may be predisposed to develop AD later in life. These studies will allow us to identify better diagnostic markers and therapeutic targets and enable early intervention to prevent the development and progression of AD.

NIH Research Projects · FY 2026 · 2025-06

Abstract My research program aims to understand the molecular mechanism of cell death and develop small molecular inhibitors to treat diseases associated with dysregulated cell death, including systemic inflammatory response syndrome (SIRS), infection, and heart failure. Apoptosis and necroptosis are essential pathways of cell death with distinct biochemical mechanisms, pivotal in development and disease. Apoptosis involves caspase activation, while necroptosis triggers the assembly of the necrosome, containing receptor-interacting protein kinase 1 and 3 (RIPK1/RIPK3) and the mixed lineage kinase-like protein MLKL. Despite advancements, questions persist regarding RIPK1 activation, necroptosis execution, and the contribution of necroptosis to heart failure. Through a sensitized CRISPR whole-genome knockout screen, we have discovered the essential role of protein phosphatase 1 regulatory subunit 3G (PPP1R3G) in cell death. PPP1R3G partners with PP1γ to dephosphorylate RIPK1, activating both apoptosis and necroptosis. Ppp1r3g-/- mice exhibit protection against TNF-induced SIRS, affirming its in vivo importance. However, little is known about PPP1R3G’s involvement in cardiac cell death and injury. Project 1 aims to elucidate the role of PPP1R3G in myocardial infarction (MI) and doxorubicin (DOX)-induced cardiac toxicity, enhancing our understanding of cardiomyocyte death and its therapeutic implications. Furthermore, we have developed a novel peptidomimetic that disrupts the interaction between PPP1R3G and PP1γ, blocking cell death in vitro and protecting against TNF-induced SIRS. In Project 2, we will further investigate its mechanism of inhibition and explore its efficacy in mouse models of MI and DOX-induced cardiotoxicity. Project 3 focuses on unraveling necroptosis execution mechanisms. While MLKL is traditionally believed to oligomerize on the plasma membrane, our recent findings suggest that significant portions of MLKL polymerizes on the lysosomal membrane, inducing lysosomal membrane permeabilization (LMP) and cell death. Through a CRISPR screen, we identified a novel membrane protein, that we named MADMAN for MLKL-associated membrane activator of necroptosis, as a crucial protein recruiting MLKL to the lysosomal membrane. We'll investigate MADMAN's role in necroptosis and its in vivo function in TNF-induced SIRS and MI. Our proposal employs forward and reverse genetics, biochemistry, and structure-based drug design to examine the mechanisms of cell death systematically and rigorously. The outcomes of our studies will provide innovative molecular insights into inflammation and cell death pathways and uncover potential drug candidates, paving the way for the development of novel therapeutic strategies for human diseases linked to cell death dysregulation.

NIH Research Projects · FY 2025 · 2025-06

Project Summary/Abstract The long-term objective of this application is to identify novel biomarkers for early diagnosis and/or prognosis prediction of Alzheimer’s disease (AD), a neurodegenerative disorder that affects 5.5 million people in the US. This is consistent with the mission of NIA. This proposal aims to determine brain extracellular matrix (ECM) composition changes during normal aging and in AD in both rodents and humans using an innovative decellularization-based proteomic approach. In Aim 1, Mouse ECM composition in different brain regions and at various ages will be determined using an innovative decellularization-based proteomic approach optimized in our laboratory. In Aim 2, brain ECM composition changes in both 5xFAD and PS19 mouse models of AD will be investigated similarly. Different brain regions and various ages (representing distinct stages of AD) will be analyzed to determine any region-specific and age-dependent changes. In Aim 3, ECM composition alterations in human AD brains will be explored using postmortem prefrontal cortex samples from AD patients and age/gender-matched controls. In addition, the contributions of CAA (a vascular pathology frequently found in AD brains) and ApoE4 (a major genetic risk factor for AD) in ECM composition will be determined by including samples with and without CAA and ApoE4 in each condition. Successful completion of this study will establish ECM composition in mouse brains in a region-specific manner, elucidate ECM changes during normal aging, characterize the temporary and spatial changes of the ECM in two mouse models of AD, and determine ECM alterations in AD patients. These findings will provide a comprehensive picture on how each ECM protein changes during normal aging and in AD in any brain region at any time, which will pave the way for future research and substantially move the field forward. This proposal may lead to the identification of novel biomarkers in early AD diagnosis and/or prognosis prediction.

NSF Awards · FY 2025 · 2025-05

An effective wastewater infrastructure is vital to preventing pollutants from harming human and environmental health. Centralized sewer-based systems are expensive to install and maintain and cannot serve low-density rural areas. About 25% of Americans, or 31 million households, rely on onsite systems for sanitation. Wastewater infrastructure on islands face additional challenges, as they are subject to saltwater intrusion, shallow groundwater, poor soils, high material, labor, and energy costs, and proximity to sensitive ecosystems like coral reefs. In Hawaii alone, an estimated 83,000 households on cesspools discharge 52 million gallons of untreated sewage into the environment each day, harming public health and fragile nearshore ocean habitat. On the mainland U.S., millions of people in small, isolated rural communities in places such as Appalachia, Alabama, Alaska, and the Navajo Nation also struggle with poor sanitation stemming from inadequate wastewater infrastructure. This project will develop a new class of technologies called adaptive decentralized wastewater infrastructure solutions (ADWIS), which are capable of nutrient removal and water recycling, contain automation and remote monitoring, and are energy independent on renewable sources. Working with community partners, local wastewater professionals, and the Native Hawaiian Science and Engineering Mentoring Program, the team will broaden participation by students and researchers from underrepresented groups, and engage with communities with onsite wastewater challenges in Hawaii and beyond. A convergence research team of water professionals from academia, industry, and the non-profit sector will tackle the unique wastewater challenges of island communities. Using the islands of Hawaii as an acceleration platform, the team will develop and mature an ADWIS called Honu Hub which provides micro-grid services to a single or cluster of homes. The project is comprised of six thrusts. Thrust 1 focuses on the design, fabrication, testing, certification, and pilot demonstration of a Honu Hub in Hawaii. Thrust 2 continues research and development to decrease operational and maintenance costs. Thrust 3 intends to understand and overcome institutional barriers (regulatory, economic, behavioral) in the diffusion of new technologies like Honu Hub and ADWIS in general. Thrust 4 develops go-to-market strategies for Honu Hub. Thrust 5 promotes education and workforce development for ADWIS. Thrust 6 addresses track integration and cross track activities to achieve greater synergy across the Convergence Accelerator portfolio. The intellectual merit of the project includes the research and development of a novel circular economy-based decentralized wastewater treatment technology which can help address water quality and scarcity challenges for island communities. The anticipated outcomes and deliverables are a market-ready ADWIS which is ready to be upscaled and applied to Hawaii, other islands in the U.S. Pacific region, and mainland U.S. The broader Impacts include introducing frameworks for overcoming institutional, regulatory, and financial barriers to the adoption of new onsite wastewater solutions. 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 2025 · 2025-05

Asthma is the most common chronic inflammatory disease of the airways, affecting 24.6 million people in the US and almost 500 million worldwide. Asthmatic patients have three main characteristics: airway resistance due to narrowing of the airways, lung inflammation, and airway hyperreactivity (AHR). AHR is the excessive and inappropriate response of the airways to a bronchospastic/irritant stimulus. Current asthma medications target airway blockage and inflammation, but none adequately treat AHR. AHR is the cause of most symptoms and exacerbations of asthma and persists even if the chronic inflammation in the lungs is cleared. There is a significant gap in our understanding of the mechanisms underlying the development of AHR. House dust mites (HDM), a common trigger of asthma, cause the development of AHR and evidence suggests this is independent of IgE-mediated atopy and we found this AHR is dependent on nociceptive sensory nerves innervating the airways. However, the mechanisms and specific sensory neve populations responsible for HDM-mediated AHR are poorly understood. The long-term goal of this proposal is to define the neural mechanisms that are triggered by HDM by activating the airway afferents leading to the development of AHR, so that we can develop targeted therapies. The objective of the study is to identify the specific nerve subtype and the signaling mechanism triggered by HDM activation of the airway vagal afferents and determine the mechanism by which AHR eventually develops. The central hypothesis is that HDM component proteases cause PAR1 dependent activation, via TRPV1 and Ano1 ion channels, of vagal C-fibers which leads to the development of HDM-induced AHR. To address the hypothesis, we have three specific aims: Aim 1: Determine the protease-mediated mechanism of HDM-evoked airway afferent activation and AHR. Aim 2: Determine the afferent effectors underlying HDM- mediated afferent activation and AHR. Determine the contribution of chronic activation and phenotypic changes in afferents to HDM-evoked AHR. We hypothesize that the development of HDM-induced AHR in mice is due to the activation of the TRPV1 and Ano1 ion channels, expressed on airway vagal afferents, downstream of PAR1 activation. The rationale of this proposal is that once we understand the mechanisms, we will be able to treat AHR. This R01 will be significant because it this proposal will be the first to define the afferent subset and the molecular mechanisms necessary for triggering AHR in a translationally relevant HDM mouse model of AHR. This R01 research proposal is innovative because it (1) investigates the initial responses to HDM that are sufficient to cause AHR independent of inflammation, (2) hypothesis that HDM components directly activate naïve airway afferents which then lead to AHR, is innovative. The outcomes of this study will provide a novel rationale for pharmacological or electroceutical therapies that target airway afferent nerves hence treating the condition, for the first time, of AHR in clinical studies.

NSF Awards · FY 2025 · 2025-05

Non-technical: The light emitting diode (LED) is a crucial opto-electronic device which has transformed modern lighting technology as well as high- speed communications based on optical-fibers. In standard LEDs, electrons and the absence of electrons, termed holes, are injected from metallic contacts into opposite ends of a semiconductor junction, where they recombine to generate a photon. The recombination process, and hence the light intensity, can be quickly modulated for information encoding and communications. This project aims to also control the spin of the injected electrons, adding an additional degree of freedom to the information encoding through efficient modulation of the light circular polarization. Spin is a fundamental property of an electron, as is the electron’s charge and mass. Spin injection into semiconductors is challenging because of the large mismatch of electrical resistance between common magnetic metal electrical contacts and the semiconductor. The project will explore magnetic electrical contacts comprised of a class of materials termed ferrimagnetic rare earth / transition metal (RE/TM) alloys that can reduce this electrical resistance mismatch, and thereby greatly improve spin injection efficiency. Different combinations of two-dimensional semiconductors, almost atomically thin, with spin-selective light polarization emission, will be tested. Changing the magnetic state of the RE/TM contacts, even within very short time scales, reverses the injected electron’s spin and hence the circular polarization (left or right) of the emitted light. The results of this project can lead to innovative new technical capabilities including ultrahigh speed optical communications, three-dimensional displays, quantum encryption and other quantum information applications, and secure long-range communication. The research will support two graduate students and will expose numerous undergraduates in advanced research methods. Technical: This project will combine electronics, spintronics, valleytronics and photonics into an integrated device that can serve as an efficient, electrically controlled emitter or sensor for circularly polarized photons. At the heart of the proposed device structure are thin layers of two-dimensional (2D) semiconductor transition metal dichalcogenides (TMDs), such as WSe2 or MoS2. Single layer TMDs have a crystal structure that lacks in-plane inversion symmetry, leading to an electronic band structure characterized by spin-inequivalent valleys at distinct points in momentum space (K and K’ points). This close connection of spins and electronic band structures is an example of spin-momentum locking. For light emission applications, spin polarized carriers will be injected from metallic magnetic electrodes, thereby disproportionately populating the K or K’ points. The project focuses on two important advances: (1) use of tunable and low work function ferrimagnetic electrodes, namely Gd based rare earth / transition metal (RE/TM) alloys, to greatly improve the spin injection into the TMDs; and (2) growth of lateral TMD-1 / TMD-2 heterojunctions (e.g. MoSe2 / WSe2) with dissimilar p-doping and n-doping, which then naturally form nearly-perfect, one dimensional p-n junctions. The spins injected at the ferrimagnetic electrode will diffuse to the p-n junction, recombine with holes across the junction, and emit chiral (circularly polarized) photons. Reversing the magnetization of the ferrimagnet will reverse the sign of the injected spins and hence reverse the photon chirality. Several materials optimization steps will be needed to achieve this result, and the project will also develop precision optical magnetic metrology methods based on the spin Hall effect of light (SHEL) to better understand the diffusion length and lifetime of the injected spins. The results will establish a new class of 3D / 2D heterostructures for opto-spintronic applications. 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.

NSF Awards · FY 2025 · 2025-05

In this project, the Department of Computer Science and Engineering at the University of South Florida (Tampa, FL) will host a summer program annually from 2025 to 2027 to train 10 students each year in computer hardware security. Over three years, a total of 30 students, particularly those from schools with limited research opportunities or from underrepresented groups, will participate in the 10-week program. During the program, students will learn the basics of computer hardware security and work on research projects related to detecting and fixing security issues in computer hardware, mentored by experienced faculty and doctoral students. The program will also include academic and social activities to help students build essential skills in research, technical writing, and communication. With computers being an essential element in many systems and infrastructures that are pivotal to national security, this program aims to prepare the future workforce capable of defending national security. Interested students can apply through NSF's Education and Training Application portal: https://etap.nsf.gov. This program on hardware security offers undergraduate students from diverse backgrounds the opportunity to participate in high-caliber research projects with mentorship from faculty and graduate students. Students will be engaged and involved in state-of-the-art and challenging research problems that are fundamental to complex system security assurance. Students will learn the critical concepts and knowledge of computer hardware security problems and their implications. They will be introduced to recent advances in hardware security vulnerabilities, their countermeasures, and other assurance methods. All students will present the results of their research in a poster competition and at a university-wide research symposium. By engaging women and individuals from underrepresented groups, the program seeks to broaden participation in computing, and to prepare them to successfully tackle a job or pursue advanced degrees in Computer Science and Engineering or a related field. To measure the program’s success, the Computing Research Association’s Center for Evaluating the Research Pipeline (CERP) will help assess its outcomes. 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.

NSF Awards · FY 2025 · 2025-05

Ctenophores, commonly called comb jellies, are gelatinous animals that are significant predators in the world’s oceans. Because of their key predatory role in ocean ecosystems, it is important to understand how they capture prey in order to fully comprehend how they impact ocean food webs. Ctenophores are commonly thought to use sticky cells, called colloblasts, to capture prey. However, previous observations provide strong evidence suggesting that ctenophores use neurotoxic chemicals to anesthetize their prey and that this is the primary mechanism they use to capture and ingest prey. This study will investigate the role of these neurotoxic chemicals for prey capture by ctenophores by quantifying (a) how these chemicals incapacitate prey, (b) how common these chemicals are among different types of ctenophores, and (c) how effective these chemicals are on different types of prey. The project is expected to yield a transformative understanding of the mechanisms behind the remarkable success of a group of seemingly fragile marine predators that are unusually successful at capturing evasive prey. Understanding these toxins may open new opportunities for therapies and drug discoveries. In fact, it is likely this research will introduce a novel class of reversible anesthetic compounds. The nature of the research will foster engagement of many students in marine science, chemistry, and biomedicine. Ctenophores, dominant marine zooplankton in coastal and oceanic ecosystems, can significantly impact global food webs through top-down control of zooplankton populations. Traditionally, their predatory success was attributed to adhesive cells (colloblasts) used for prey capture. However, new evidence reveals that ctenophores primarily rely on neurotoxic chemicals in their mucus to anesthetize prey, reshaping our understanding of their feeding strategies and prey selection. This project aims to investigate how ctenophore mucus toxins incapacitate prey, toxin prevalence across ctenophore species, and their effectiveness on various prey types. Objectives include: (a) measuring mucus effects on different prey taxa, (b) assessing how mucus influences prey retention and selection in target species, (c) determining the taxonomic distribution of toxic mucus among ctenophores, and (d) exploring the mechanistic basis of prey immobilization via mucus-ion channel interactions. This research is expected to yield a transformative understanding of the mechanisms behind the remarkable success of ctenophores that are unusually successful at capturing evasive prey. Understanding the action of ctenophore mucus toxins may open new opportunities for therapies and drug discoveries. In fact, it is likely this research will introduce a novel class of reversible anesthetic compounds. The nature of the research will foster engagement of many students from marine science to chemistry to biomedicine. 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.

NSF Awards · FY 2025 · 2025-04

In recent years there have been increasing calls from fields such as medicine to expand the use of digital technologies in providing healthcare in low-resource settings. Particularly in rural areas, people may not be able to easily visit a healthcare provider in person, but they often have access to devices such as mobile phones. This project examines efforts to develop digital health services in a low-resourced and predominantly rural setting. The research contributes to the improvement of digital health services, offers training for graduate students, postdoctoral scholars and undergraduate students, and enhances the infrastructure for research and education. This study addresses the following interrelated questions: (1) How do digital health technologies create new treatment experiences? (2) How do they affect communication strategies and relationships between patients and providers and (3) Are they considered an effective means of delivering treatment by providers and patients? Methods include the use of in-depth interviews and behavioral observations across a stratified sample of healthcare providers in three organizations, with patients and their family members. This project allows a rare opportunity to explore experiential dimensions of communication and human-technology interfaces. The long-term contribution to the science of medicine is an understanding of how new health technologies remake treatment strategies and patient-provider relationships, and how these processes affect whether therapies are considered effective. An emphasis on provider and patient interactions also moves forward investigation of robustness as a theoretical concern in the health sciences. 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 · 2025-04

Project Summary Natural products have a long history of use in modern medicine but have recently declined as a proportion of New Chemical Entities advancing to clinical use. Among the serious challenges of natural product discovery studies is the re-isolation of known and well-studied chemotypes, despite the fact that the vast majority of biodiversity has not been subject to chemical analyses. Less than 20% of octocoral species, for example, have natural products reported in MarinLit, the foremost database of marine chemistry. After sponges, octocorals are the primary source of bioactive and structurally unique marine natural products. One reason for the disparity in chemical analysis of octocorals is that many unstudied or understudied specimens are difficult to access, inhabiting environments such as the deep sea, polar waters or in geopolitically problematic regions. To address the limited access to underrepresented marine organisms, we propose to study the marine invertebrate holdings of natural history museums (NHM’s). With recent advances in analytical instrumentation and analysis platforms, it is increasingly possible to characterize low levels of metabolites. Orbitrap and QToF mass spectrometers, coupled with nanoflow liquid chromatographs, are capable of separation and highly accurate mass measurements of even trace metabolites in complex mixtures. Bioinformatic platforms such as MZmine are adept at deconvoluting mass data to identify individual features (~molecules and their fragmentation products), which can then be parsed by e.g. SIRIUS, which uses machine learning and database comparisons to interpret those features and predict structural fragments or even de novo putative structural assignments. Validation of putative structures from mass data can be achieved even in mixtures with targeted NMR sequences such as PSYCHE-TOCSY and DREAMTIME. Further, computational approaches such as Density Functional Theory (DFT) provide chemical shift predictions that can be used to propose stereochemical assignments. These advances open the door to vigorous analysis of samples archived in NHM’s, samples that span both geographic and temporal space that is often inaccessible to chemist-collectors. Not only do NHM’s provide diverse samples, but the samples are identified by experts in their field and they are geotagged and fully permitted. The Smithsonian Institution’s National Museum of Natural History (NMNH) maintains a warehouse with decades to more than a century of collections of ethanol-preserved marine invertebrates. Sampling the ethanol from several coral species in the NMNH, our preliminary analysis demonstrates the potential of these samples to yield new natural products. This project seeks to validate the NMNH samples as a significant drug discovery resource by identifying new metabolites in one well known coral species as well as characterization of new chemotypes from one or more previously unstudied coral species.

NSF Awards · FY 2025 · 2025-04

This project addresses the following questions: How do movers who have left their homes after a natural hazard adapt to and integrate into their new communities over time? How do those movers’ social statuses and identities shape adaptation and integration experiences after post-disaster population movement? In what ways do movers create meaning in new places of residence, and under what conditions do they remain settled or return to the disaster-stricken place? Answers to these questions are important because they can reveal what elements of a destination place are conducive to long-term settlement, and the conditions under which movers can successfully rebuild their lives after a disaster uproots them. The Principal Investigator (PI) will answer these questions by interviewing post-disaster movers about their experiences recovering and rebuilding their lives after moving to a new place. The PI will locate and interview study participants who were surveyed and interviewed in 2020 after their post-disaster movements, to understand what opportunities and challenges they have encountered in their new communities since these interviews took place. This study advances knowledge and scholarship by using novel longitudinal data to examine how movers rebuild their lives after disaster-induced population movement, focusing on the role of destination places in shaping long-term settlement decisions. Aligned with NSF’s mission, this project addresses the intersection of population movement, disaster response, and social integration to promote societal welfare and scientific progress. Additionally, it promises to benefit society by informing more effective incorporation strategies and support services for movers in disaster-prone areas. The project focuses on movers after hurricanes compromised their homes in 2017 and beyond. The study explores how demographic characteristics influence movement in order to better understand the relationship between place- and home-making processes and societal incorporation. By re-interviewing a sample of 54 movers, including a sub-sample of return movers, this project will be the first to longitudinally examine post-disaster population movement, capturing not just multi-level factors influencing incorporation and settlement, but return movement and resettlement and factors that shape re-adaptation. Data collection will involve 2–3-hour in-depth interviews conducted in participants’ homes or other significant community spaces. Understanding post-disaster population movement will illuminate broader patterns and processes relevant to other disaster-prone regions globally. 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 2024 · 2025-04

PROJECT SUMMARY/ABSTRACT Nurses represent the largest numbers of health care workers. As a critical component of the health care workforce, nurses must have a strong foundation in genomics. This is particularly true for faculty preparing the next generation of nurses to provide clinical care and conduct research. Advances in genomic science are redefining our understanding of health and illness, necessitating a concomitant shift in nursing education and 1 practice. A goal of the nursing profession, highlighted in the Institute of Medicine Future of Nursing report , is to increase the number of nurses with doctoral degrees to ensure that sufficient numbers of faculty are available to prepare the nursing labor force needed for delivery of health care services. Doctoral-prepared nurses with terminal degrees of DNP and PhD have opportunities to lead change in health care systems and transform care with the translation and integration of genomics in education, scholarship and practice. The purpose of this educational project is to improve the knowledge and skills of doctoral nurses in medical genomics. The need for the project was identified through a literature review and targeted needs assessment of nursing faculty and students. The project will commence with a half-day medical genomics course provided as a preconference at the American Association of Colleges of Nursing annual doctoral conference followed by monthly webinars and web conferencing sessions for the remainder of the year. The project will use the training-of-trainers model2 to disseminate information and strategies to implement genomics nursing education and is expected to prepare at least 200 additional "trainers" in medical genomics over the course of five years. These trainers will translate and integrate genomic information in nursing academics, scholarship and practice to serve as genomic champions at their schools of nursing. The primary aims of this proposed educational project are to: 1) develop and implement educational programs and materials aimed to achieve competency in medical genomics for doctoral nurses. 2) prepare doctoral nurses to integrate genetic and genomic content into academics and clinical practice; and 3) determine areas of strengths and weaknesses of doctoral nurses in foundational genomic concepts to inform future educational planning. The course offers didactic and experiential training as well as written and online resources, to facilitate the translation and integration of genomic content. Ongoing program evaluation will guide subsequent courses to address gaps in understanding and barriers to implementation. Doctoral nurses will obtain knowledge and skills to incorporate genomic medicine into academic curricula as well as in research and clinical practice. This educational program in medical genomics builds on the investigators' collective experience with educational endeavors in genomics and is an educational collaboration between the investigator/s and the American Association of Colleges of Nursing (AACN).

NSF Awards · FY 2025 · 2025-02

This doctoral dissertation research studies the social and environmental impacts of energy transitions on coastal communities. The investigators specifically test how community decision-making and adaptations impact local regions impacted by energy transitions. The research expands scientific understanding of community adaptations and decision-making in the context of new, sustainable energy solutions. In addition to providing scientific training for a graduate student in anthropology and interdisciplinary research in the energy sector, the broader impacts of this research involve close collaboration with local communities in the development of educational materials on energy transitions. Research findings will also be shared to inform local adaptations to changes in the energy sector. In order to understand the lived experiences of communities most impacted by the new energy sector, investigators utilize a mix-methods approach that combines qualitative and quantitative data collection. Investigators specifically use semi-structured interviews, content analysis, and quantitative analysis of health, environment, and socioeconomic data of communities living in impacted areas of energy sector expansion. The research makes significant contributions to environmental anthropology, the anthropology of energy, and to the social science of local impacts of global energy infrastructures. 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.

NSF Awards · FY 2025 · 2025-02

The 41st edition of the Southeastern Analysis Meeting (SEAM) will be held on the campus of the University of South Florida, March 21-23, 2025. SEAM has been held annually at a university in the southeastern United States since 1985. It has established itself as leading national venue for analysis, with a mission of promoting interaction and collaboration between researchers at all career stages. It encourages research and education in the field of analysis. The program of SEAM includes plenary talks by selected participants and 20-minute contributed talks open to all participants as well as professional development activities for early career researchers. This format fosters collegiality and a vibrant environment that encourages the exchange of ideas, networking, and the initiation and development of new research collaborative projects. The Southeastern Analysis Meeting (SEAM) promotes interaction and collaboration between researchers at all career stages and encourages research and education in the field of analysis. The meeting brings together experienced researchers, junior faculty, postdocs, and graduate students to discuss recent work and advances in analysis, classical and modern — the mathematics at the intersection of Operator Theory, Classical Complex Analysis, Harmonic Analysis, and Several Complex Variables — and related areas and fields of application, including Operator Algebras, Spaces, and Systems; Systems and Scattering theory; Control Theory; and PDE to name a few. As an annual event with a dedicated focus, it is now a part of the research community infrastructure, enhancing research in mathematics and graduate education, as will be described in further detail throughout this proposal. The meeting website is at https://www.usf.edu/arts-sciences/departments/mathematics-statistics/research/conferences/seam2025/index.aspx 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 · 2025-02

Cardiovascular diseases (CVD) are the leading causes of death worldwide. Although diagnosis and treatment approaches have improved, the prognosis of heart failure (HF) patients remains poor. After myocardial infarction (MI), there is a permanent loss of functional cardiomyocytes (CMs), and as the mammalian heart has limited regenerative capacity, it leads to HF and death. Lower organisms like zebrafish, newts, and even 1-day mice and pig can regenerate their heart post-injury by inducing CM proliferation. Attempts have been made to transiently reconstitute embryonic signaling in adult hearts, including overexpression of cell cycle activating and proliferative genes, with limited success. Existing gene therapy approaches for the heart have significant challenges like short-term, low, or uncontrolled expression and genome insertion, resulting in insufficient CM proliferation and cardiac repair. Recently we have shown that modified mRNA (modRNA) delivery is a safe, efficient, transient, non-immunogenic, local, and dose-controlled gene delivery platform for the heart. Induced pluripotent stem cells (iPSC)-derived extracellular vesicles (EV)/exosomes have been shown to improve cardiac function. However, the mechanism of iPSC-EV mediated cardiac regeneration remains unclear. In our preliminary studies, using a hiPSC-extracellular proteomic approach combined with a developmentally restricted gene database of mouse hearts, we identified for the first time that Phosphoserine Aminotransferase 1 (PSAT1) protein is expressed exclusively in hiPSC-EVs, and PSAT1 mRNA expression is significantly downregulated quickly after the postnatal period in mice hearts. Myocardial delivery of PSAT1 modRNA induced CM proliferation, improves cardiac function and mice survival post-MI. Furthermore, we showed that YAP1 is a transactivator of PSAT1 and induces its expression, and in turn, PSAT1 induces β-catenin nuclear translocation to induce CM proliferation. We found a novel YAP1-PSAT1-β-catenin molecular signaling axis in cardiac regeneration. Moreover, PSAT1 induced serine synthesis pathway (SSP), nucleotide synthesis and inhibited oxidative stress and DNA damage response post-MI. This proposal will determine a local and short pulse of cmsPSAT1 (CM-specific PSAT1) or PSAT1 modRNA is sufficient for the induction of cardiac regeneration and reversal of cardiac remodeling post-MI and HF, respectively, and will study the pleiotropic effects of PSAT1 through novel molecular mechanisms on activating YAP1-β-catenin molecular axis and downstream signaling pathways. Finally, determine the involvement of SSP in PSAT1 induced CMs proliferation and cardiac regeneration post-MI. The highly translatable nature of our proposed modRNA platform and our integrative, multi-disciplinary experimental plan are ultimately geared towards clinical applicability for ischemic heart diseases.

NIH Research Projects · FY 2026 · 2025-01

This grant initiative undertakes an exploration of Reelin, an extracellular signaling protein, and its role in Fragile X syndrome (FXS). FXS is the most prevalent inherited form of intellectual disability, that manifests with a spectrum of clinical symptoms including impaired cognition, anxiety, hyperactivity, social phobia, and repetitive behaviors. FXS has an estimated prevalence of 1 in 7,000 males and 1 in 11,000 females (Centers for Disease Control). The core pathology of FXS stems from loss-of-function mutations in the X-chromosome gene FMR1, resulting in a lack of FMRP (Fragile X Messenger Ribonucleoprotein Protein) expression. FXS remains an enigmatic challenge, devoid of a cure, with available medications merely aimed at mitigating specific symptoms, such as anxiety, hyperactivity, aggression, and attention deficits. As a single-gene disorder, FXS stands out as a promising candidate for viral-vector-based gene therapy, however, the Fmr1 gene therapy approach has not resulted in the amelioration of phenotypical behaviors as anticipated. Many studies failed to report cognitive tasks or show cognitive recovery despite successful FMRP expression. Considering that the loss of FMRP function results in the disturbance of typical synaptic signaling, the goal of restoring synaptic function emerges as a compelling alternative therapeutic avenue for FXS—a terrain yet uncharted. Reelin offers a potential therapeutic target as it has emerged as a pivotal player in orchestrating synaptic dynamics. Our lab’s focus on neurodevelopmental disorders led us to identify 50% reduction in Reelin in the FXS mouse model. The tantalizing prospect that a decline in Reelin might underpin the synaptic dysregulation in FXS, we hypothesized that restoring Reelin signaling would improve synaptic signaling in FXS. Subsequently, we published that Reelin supplementation was able to fully rescue cognitive deficits in the FXS mouse model. As a follow up, we now demonstrate that an optimized minimal active Reelin fragment can also completely rescue cognitive deficits in the FXS mouse. More importantly, this construct can be expressed using a gene therapy approach, to amazingly completely restore the cognitive deficits in the FXS mouse model back to wild-type performance levels. In this proposal we further validate this gene therapy approach in Aim 1 with examination of new viral vectors that offers a less invasive gene delivery for the brain. We hypothesize that this will be as efficacious as our preliminary data, and could enhance the translatability towards a human therapeutic. In Aim 2 we will endeavor to determine the mechanism of action of Reelin in FXS. Currently there is no known direct interaction between Reelin and FMRP, but we hypothesize that Reelin indirectly rescues FMRP loss through the regulation of the synaptic proteins such as STEP and PSD-95. We will take an unbiased approach to examine the mechanism of increased Reelin signaling in Fmr1 KO mice using RNAseq and biochemical analysis of treated versus control mice.

NIH Research Projects · FY 2026 · 2025-01

Abstract Borrelia burgdorferi (Bb), the etiological agent of Lyme disease, maintains itself in nature via a complex life cycle involving an arthropod (tick) vector and small mammals. During its cycle between ticks and mammals, Bb undergoes dramatic adaptive changes in order to interact with and adapt to these two disparate niches. Previously, we discovered that BosR, a Fur/PerR homologue, plays a central role in regulating virulence gene expression and Bb pathogenicity. Our data showed that BosR is required for Bb's tick-mammal transmission as well as the establishment of mammalian infection. Moreover, we found that BosR regulates expression of rpoS. In addition, our preliminary findings revealed that (i) BosR has much broader biological relevance to Bb’s infectious cycle other than regulating rpoS expression; (ii) there is a unique mechanism(s) involved in the regulation of bosR expression in Bb; and (iii) distinct from other Fur family members, BosR employs a novel mechanism for DNA-binding and gene regulation. These combined data give rise to our hypothesis that BosR acts as an atypical Fur family member to modulate expression of Bb virulence determinants. This hypothesis will be addressed in three Specific Aims. In Aim 1 of this proposal, we will define the BosR regulon and characterize the contributions of BosR-regulated genes to Bb's infectious cycle. In Aim 2, we shall examine the biological roles of the cis-regulatory elements upstream of bosR. Through promoter deletion, reporter assay, and tick- animal infectious studies, we will decipher the roles of the cis-elements in in vivo gene expression and Bb's behavior in ticks and animals. In Aim 3, we shall determine the structure of BosR to elucidate the molecular bases underlying BosR's unconventional activities such as metal coordination and DNA interaction. These combined studies will (i) provide a transformative understanding of the in vivo importance of the BosR regulon; (ii) define the unique aspects of BosR; (iii) clarify the novel mechanism by which BosR controls Bb's virulence; and (iv) reveal new paradigms in bacterial gene and virulence regulation. Resultant findings could lead to the development of new strategies to prevent and/or treat Lyme disease.

NSF Awards · FY 2025 · 2025-01

The emerging satellite networks will play a vital role in next-generation networked systems and applications (e.g., 6G, the Internet of Things), and ensuring the reliability and security of these satellite-enabled systems and services is vital. Although generic security protocols exist, the unique characteristics of satellite systems, like delay-awareness, error-proneness, and the intricate software/network stack of space-aerial-terrestrial integrated networks (SATIN), require efficient and lightweight network security protocols. The security threats due to emerging quantum computers and the heavy overhead of existing post-quantum secure standards compound these challenges. In this project, the research team aims to fill these gaps by developing a fast and lightweight network security fabric that respects the needs of trustworthy next-generation SATIN for the post-quantum era. The team will innovate on multiple fronts, including algorithmic (quantum-safety, distributed computing, time-disclosed cryptography), architectural (decentralized SATIN, distributed key management), and evaluation aspects of SATIN. The project's broader significance lies in novel solutions that achieve delay awareness, post-quantum security, and energy efficiency for SATINs, which enhance national security and broadly offer new educational and publicly adaptable tools with international collaborations. The research team will create efficient network security solutions that increase the resiliency of next-generation SATIN to a vast range of threats, such as active adversaries, system breaches, and network faults while offering post-quantum security. The first thrust will enable delay-aware and secure broadcast functionalities by innovating post-quantum cryptography standards via new offline-online transformations, distributed execution strategies, and algorithmic improvements. The second thrust will exploit the architectural capabilities of the terrestrial segment to mitigate the quantum-safe commitment generation and distribution burden while enabling resilient key management. The third thrust will create novel and publicly verifiable symmetric-key solutions via synergizing time-disclosed cryptography and distributed computation methods. The final thrust will be to develop a comprehensive performance evaluation framework with simulations and tests (e.g., over NSF FABRIC) for our proposed network security assets that encapsulate several satellite-enabled applications and software-defined network architectures. The research team will execute outreach and broadening participation activities, including interdisciplinary curriculum development, international collaborations with workshops and joint educational activities, summer camps for minority K-12 students, industrial partnerships for transition to practice, and open-source platforms for reproducibility and broad adaptation. This collaborative U.S.-Swiss project is supported by the U.S. National Science Foundation (NSF) and the Swiss National Science Foundation (SNSF), where NSF funds the U.S. investigator and SNSF funds the partners in Switzerland. 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 · 2025-01

Stretch-sensitive esophageal vagal afferent nerves provide essential sensory feedback to brainstem interocep- tive and motor circuits that control swallow and esophageal peristalsis. Dysfunctional control causes dysphagia, ineffective motility, excessive reflux, and pain. Dysphagia is a risk factor for aspiration pneumonia in neurological and neuromuscular diseases; and excessive reflux causes heartburn in 20% of the US population, one third of which are refractory to therapy. Although the mechanosensitivity of esophageal vagal afferents has been char- acterized into low threshold and high threshold mechanoreceptor fibers, there is a fundamental gap in our un- derstanding of the receptors and/or ion channels responsible for mechanotransduction, action potential (AP) initiation and conduction in esophageal afferents. This significantly hinders our understanding of an essential physiological process in health and disease, prevents rational therapeutic targeting of its components in esoph- ageal dysfunction, and conceals serious esophageal side-effects for future therapies targeting excitability in pain, cough and epilepsy. This gap is due to two reasons: previous mechanosensitive channels have been shown to play limited roles, but Piezo channels have not been tested; and most studies of voltage-gated Na+ channels (NaV1s) required for vagal APs have focused on the cell body with its overwhelming NaV1.7 currents, rather than at the peripheral terminal or axon, thus have overlooked essential roles of NaV1.1, 1.2, 1.6 and 1.8. Our long- term goal is to exploit mechanisms of afferent feedback to improve function in esophageal disorders. The objec- tive here is determine the mechanosensitive channels and NaV1s responsible for transducing esophageal stretch into vagal afferent activation. Our central hypothesis is that stretch-evoked afferent activation is dependent on afferent Piezo channels, whose activation induces AP initiation at the esophageal peripheral terminal and AP conduction within vagal axons via unique interactions of multiple NaV1s. In Aim 1, we will identify the mechani- cally-sensitive receptors required for stretch-evoked activation of esophageal vagal afferents. Our data shows that Piezo2 and Piezo1 are required for mechanotransduction in these afferents. In Aim 2, we will determine the NaV1 channels required for the transduction of mechanical stretch into the initiation of AP from esophageal vagal afferent terminals. Our data shows that AP initiation depends on a combination of NaV1.1, 1.2, 1.6 and 1.7, via non-redundant cooperation with NaV1.8. In Aim 3, we will determine the NaV1 channels required for AP conduc- tion in esophageal vagal axons. Our data shows that NaV1.2, 1.6 and 1.7 cooperate with NaV1.8 in a frequency- dependent manner. Our technical innovations allowing for the study of AP terminal initiation and axonal conduc- tion separately were essential in the development of novel concepts of location-specific NaV1 isoform contribu- tions and of functional cooperation between NaV1.8 and other isoforms. This study will identify the ion channels responsible for the transduction of esophageal stretch into afferent activity, a process essential for life, provide targets for esophageal dysfunction and provide esophageal context for targeting excitability in other diseases.

NIH Research Projects · FY 2026 · 2024-12

Hypertension is the most significant health burden for society in terms of economic and health costs due to the increased risk for cardiovascular disease (CVD) such as myocardial infarction and stroke. Patients with hypertension have significantly greater risks for cardiovascular mortality and morbidity compared to age matched normotensive subjects, even when the patient’s blood pressure is controlled with medication. Therefore, the long-term goal of our application is to investigate the core mechanism of vascular remodeling associated with hypertension so that an effective add-on therapy can be explored for patients with hypertension. Metabolic shift to glycolysis has been recognized in many types of CVD including hypertension. However, limited information is available regarding the types of cells influenced, if it contributes to hypertension or remodeling, as well as critical mechanisms involved. The renin-angiotensin system (RAS) is considered to play a central role in hypertension as well as the associated cell phenotypes including a metabolic shift to glycolysis. While the RAS affects a variety of cells, and hypertension demonstrates a complex pathophysiology, our published data with vascular smooth muscle cell (VSMC) AT1A receptor deficient mice have demonstrated a critical role of VSMC signaling in angiotensin II (AngII)-dependent vascular remodeling. Accordingly, in this application, we will explore the essential glycolytic enzyme pyruvate kinase M2 (PKM2) activation in VSMC via AngII that uniquely mediates vascular remodeling and hypertension involving alterations in conductance as well as resistance arteries. Based on promising preliminary data, we propose a central hypothesis that the VSMC PKM2 mediates hypertension and vascular remodeling in conductance and resistance arteries, which likely involves both metabolic and non-metabolic effects via its pyruvate kinase and specific protein kinase activities. Three specific Aims are proposed to explore the vascular mechanisms and the relevance of their signal communication utilizing an AngII model of hypertension as well as aortic VSMC and fibroblasts in vitro. Aim 1 will study involvement of PKM2 activation in VSMC in hypertension and vascular remodeling. Aim 2 will study novel mechanisms of how PKM2 activation in VSMC, glycolysis dependently and independently, mediates hypertension and vascular remodeling. Aim 3 will explore VSMC-to-fibroblast communication in hypertensive vascular fibrosis via VSMC PKM2 mediated hypertension-associated secretory phenotype (HASP) including Esm1. To study the cell type and mechanism by which PKM2 is involved in hypertension and hypertensive vascular remodeling, we will utilize genetically or pharmacologically altered mice infused with AngII. Accomplishing the proposed aims will yield significant advancement of our knowledge and understanding of the mechanisms leading to the development of hypertensive vascular remodeling and provide future translational research leading to new therapies.

NSF Awards · FY 2024 · 2024-12

Wind and wave-driven Langmuir circulation (LC) or Langmuir turbulence in the upper ocean mixed layer and in unstratified shallow continental shelf regions has been extensively studied via field measurements and numerical simulations. However, studies of Langmuir turbulence in the inner shelf under the influence of the surf zone are lacking. The overarching goal of this project is to investigate numerically the structure and intensity of Langmuir turbulence and its impact on cross-shore scalar transport in idealized shallow coastal shelf environments extending from the surf zone to the inner shelf. This will require turbulent eddy-resolving simulations that can capture interactions between the Langmuir turbulence regime and common nearshore processes such as (1) pressure gradient-driven alongshore currents (e.g., tidal, and geostrophic currents), (2) transient rip currents and associated longshore currents generated by breaking waves and (3) cross-shore currents induced by diurnal surface heat fluxes. Simulations will extend over a surf-shelf transition cross-shore region of ~2 km, spanning depths between 0.1 m and ~15 m. The eddy-resolving simulations will be based on novel application of the detached eddy simulation (DES) methodology, well-established in the aerospace engineering community, to be extended to coastal ocean turbulence. The unsteady DES will be able to capture rip currents emanating from the shore while modeling the wave-breaking turbulence and other wave-related phenomena such as wave bottom and surface streaming via well-established techniques developed by the nearshore circulation modeling community. Nearshore regions are biologically highly productive and the turbulence dynamics to be studied have direct impact on physical, chemical, and biological processes affecting this productivity. Ultimately understanding nearshore turbulence dynamics is important for managing natural and economic coastal resources. This project will promote the use of DES within the physical oceanography community for continued application to understand the turbulence driven by simultaneously occurring mechanisms in the surf-shelf transition zone of the coastal ocean. Results of the proposed project will be communicated at conferences (Ocean Sciences Meeting and the Annual Meeting of the American Physical Society / Division of Fluid Dynamics) and through publication in peer-reviewed journals. The project will support a graduate student and a postdoctoral fellow, who will train in physical oceanography, turbulence dynamics and closures and numerical techniques. Although episodes of Langmuir turbulence on the inner shelf have been reported in the literature, interactions between this turbulence regime and classical nearshore processes have not been identified. This project aims to address this knowledge gap by uncovering, for example, interactions between LC and transient rip currents and the influence of LC on cross-shore scalar transport. Specific objectives of the research include: (1) To determine how far can Langmuir turbulence extend to the nearshore before it is arrested by the surf zone turbulence due to wave-breaking and whether LCs can contribute to onshore transport induced by wind and waves. (2) To elucidate the potential generation of Langmuir turbulence via tilting of vertical vorticity associated with lateral shear induced by rip currents into wind-aligned LC. (3) To determine the role of Langmuir turbulence and the hybrid regime consisting of Langmuir turbulence and bottom-generated turbulence on cross-shore scalar exchange induced by rip currents and baroclinic cross-shore currents (induced surface heat fluxes). 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 · 2024-11

Project Summary/Abstract Plasmodium falciparum is the major global cause of malaria morbidity and mortality and is especially devastating in pregnant women and children in sub–Saharan Africa. Anopheline mosquitoes are essential for the spread of new infections, requiring ingestion of mature sexual stages from an infected person and then a second blood meal once infectious sporozoites are in the mosquito salivary glands. Development of sexual stages in an infected person’s blood cells requires a complex ~14-day development phase. Even with a lot of recent progress, many processes essential for sexual stage development remain poorly understood. Our group has developed a functional genomics approach using random piggyBac mutagenesis, which can be applied at genome scale to identify the P. falciparum genes essential for gametocyte development. We used this approach to complete the first saturation mutagenesis screen of P. falciparum to functionally annotate genes essential and dispensable for asexual blood-stage development. We estimate many genes in the cryopreserved saturation mutagenesis library are likely to be sexual-stage genes and this mutant library can be used for a forward phenotypic screen to identify most genes needed for sexual stage development. Advanced ‘omics analyses of selected mutants will be used to validate phenotypes and elucidate the broader cellular events that underlie the phenotypes during sexual stage development in infected human blood cells. The project combines expertise in gametocyte biology, advanced computational genomics, and phenotype comparisons with clinical isolates.

NSF Awards · FY 2024 · 2024-10

This project follows engineering graduate students, professors, and those in industry to learn about their experiences when it comes to the climate they face in engineering and the factors that relate to their persistence. Specially, this research involves multiple explanatory angles to understand persistence, including the knowledge and beliefs engineers have, the people whom they go to for advice and resources, and the climate they experience in engineering. This advances scientific knowledge about the multiple intersecting phenomena that shape social trends when it comes to how the engineering workforce (industry and academia) does not represent the broader U.S. population demographically. This knowledge can help craft more inclusive engineering environments and broaden participation in the field. A more representative engineering workforce can improve society in multiple ways, such as by supporting advancements in engineering practice and education made possible by diverse perspectives therefore making peoples’ lives better both inside and outside of the academy. This study builds upon an existing dataset, following a previous cohort. The project revisits approximately 2,100 participants from 11 universities who were enrolled in their first year in an engineering degree program in 2014. The previous project followed them for five years through annual surveys and two rounds of interviews with a subsample of 55 women and underrepresented students. In the new project, we follow the large cohort again using two more surveys, and also conduct interviews this time expanded to a total of 120 interviewees. Altogether, the new project expands the dataset into what will become a 12-year longitudinal project that began with students reflecting on their last year of high school to then following them into their first few years of graduate school or engineering occupations. The new project additionally provides outcome information for many respondents from the first study who were still enrolled in their engineering program at their fifth year. Further, the new project introduces added dimensions of identity measures (beyond binary gender as well as sexuality) to further capture how diversity is likely subsequently tied to climate and persistence. Using Ego Network Analysis, Logistic Regression, and Reflective Thematic Analysis, findings from this work can show how institutional climate intersects with cultural models and social networks to impact persistence in ways that likely vary for engineers with a range of identities, including those of race/ethnicity, binary gender, gender diverse, and sexuality. This project is supported by NSF's EDU Core Research (ECR) program. The ECR program emphasizes fundamental STEM education research that generates foundational knowledge in the field. Investments are made in critical areas that are essential, broad and enduring: STEM learning and STEM learning environments, broadening participation in STEM, and STEM workforce development. 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.