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Limited Competition: Specific Pathogen Free Macaque Colonies to Support HIV/AIDS Research (U42 Clinical Trial Not Allowed)

National Institutes of Health

Limited Competition: Specific Pathogen Free Macaque Colonies to Support HIV/AIDS Research (U42 Clinical Trial Not Allowed)

2026-09-25

research

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Limited Competition: Specific Pathogen Free Macaque Colonies to Support HIV/AIDS Research (U42 Clinical Trial Not Allowed)

National Institutes of Health

The purpose of this Notice of Funding Opportunity (NOFO) is to provide continuing support for specific pathogen-free (SPF) macaque colonies previously funded under the auspices of PAR-21-089 and PAR-18-669 that support Human Immunodeficiency Virus (HIV)/Acquired Immunodeficiency Syndrome (AIDS) research. Breeding colonies are essential to sustain appropriate SPF macaques for research related to HIV/AIDS. Pedigree SPF macaques are free of certain viruses, which may confound the results of HIV/AIDS-related investigations or present a risk to the personnel who care for the animals. The SPF macaques are genetically characterized for major histocompatibility complex (MHC) class I types, because MHC class I genotypes have large effects on macaque immune responses to Simian Immunodeficiency Virus (SIV) that can induce AIDS in nonhuman primates (NHPs) and on human immune responses to HIV.

2026-09-25

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Limited Competition: Specific Pathogen Free Macaque Colonies to Support HIV/AIDS Research (U42 Clinical Trial Not Allowed)

National Institutes of Health

The purpose of this Notice of Funding Opportunity (NOFO) is to provide continuing support for specific pathogen-free (SPF) macaque colonies previously funded under the auspices of PAR-21-089 and PAR-18-669 that support Human Immunodeficiency Virus (HIV)/Acquired Immunodeficiency Syndrome (AIDS) research. Breeding colonies are essential to sustain appropriate SPF macaques for research related to HIV/AIDS. Pedigree SPF macaques are free of certain viruses, which may confound the results of HIV/AIDS-related investigations or present a risk to the personnel who care for the animals. The SPF macaques are genetically characterized for major histocompatibility complex (MHC) class I types, because MHC class I genotypes have large effects on macaque immune responses to Simian Immunodeficiency Virus (SIV) that can induce AIDS in nonhuman primates (NHPs) and on human immune responses to HIV.

2026-09-25

Health

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Limited Competition: Stimulating Access to Research in Residency Transition Scholar (StARRTS)

National Institutes of Health

Limited Competition: Stimulating Access to Research in Residency Transition Scholar (StARRTS)

Rolling

research

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Limited Competition: Superfund Hazardous Substance Research and Training Program (P42 Clinical Trial Optional)

National Institutes of Health

The National Institute of Environmental Health Sciences (NIEHS) is announcing the continuation of the Superfund Hazardous Substance Research and Training Program, referred to as Superfund Research Program (SRP) Centers. SRP Center grants will support problem-based, solution-oriented research Centers that consist of multiple, integrated projects representing both the biomedical and environmental science and engineering disciplines; as well as cores tasked with administrative (which includes Center leadership, data management, and training); translational research and engagement; and research support functions. The scope of the SRP Centers is taken directly from the Superfund Amendments and Reauthorization Act of 1986, which limits competition for this program to accredited institutes of higher education.Please see Section III. Eligibility for additional information. In accordance with NIH standard peer-review processes, the application(s) will be peer-reviewed, and only meritorious application(s) will be considered for funding.

Up to $1.8M

2028-09-25

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Limited Competition: Superfund Hazardous Substance Research and Training Program (P42 Clinical Trial Optional)

National Institutes of Health

Limited Competition: Superfund Hazardous Substance Research and Training Program (P42 Clinical Trial Optional)

2028-09-25

research

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Limited Competition: The NHGRI Analysis, Visualization, and Informatics Lab-space (AnVIL) (U54 Clinical Trial Not Allowed)

National Institutes of Health

The National Human Genome Research Institute (NHGRI) intends to issue a Notice of Funding Opportunity (NOFO) to support a limited competition renewal of the Analysis, Visualization, and Informatics Lab-space (AnVIL) program. AnVIL is a secure, cloud-based platform that enables researchers to access, share, and analyze large-scale genomic datasets without relying on local infrastructure. Currently, AnVIL hosts more than 5 petabytes of data from nearly 300,000 research participants, providing a robust environment for reproducible, cloud-native genomic research.The renewed program will continue to advance AnVIL as a community resource grounded in FAIR (Findable, Accessible, Interoperable, and Reusable) principles. Key priorities include enhancing scalability; strengthening interoperability across a federated NIH data ecosystem; and maintaining rigorous security aligned with the Research Authentication Service (RAS) and NIH controlled-access data repositories and access management systems (CADR) requirements (see NOT OD 25 159). The renewal will also support integration of emerging data types and computational tools, including infrastructure for developing and running AI-based methods and complex analysis workflows.In addition to platform development, the program will expand training and outreach to help researchers effectively use AnVIL s multimodal datasets and reproducible analysis capabilities. By connecting secure data access, analytical tools, and workforce development, the renewed AnVIL program aims to accelerate discovery across the research lifecycle and strengthen the genomics community s capacity for clinical and translational science.This Notice is being provided to allow potential applicants sufficient time to develop responsive applications. The NOFO is expected to be published in 2027 with an anticipated application due date in 2027. This NOFO will utilize the U54 activity code.This is a Forecast for a limited competition that will invite application(s) from eligible organization(s) to apply. Please see Eligibility Section for additional information. In accordance with NIH standard peer-review processes, the application(s) will be peer-reviewed, and only meritorious application(s) will be considered for funding.

2027-05-25

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Limited Competition: The NHGRI Analysis, Visualization, and Informatics Lab-space (AnVIL) (U54 Clinical Trial Not Allowed)

National Institutes of Health

Limited Competition: The NHGRI Analysis, Visualization, and Informatics Lab-space (AnVIL) (U54 Clinical Trial Not Allowed)

Rolling

general

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Limited Competition: The NHGRI Analysis, Visualization, and Informatics Lab-space (AnVIL) (U54 Clinical Trial Not Allowed)

National Institutes of Health

The National Human Genome Research Institute (NHGRI) intends to issue a Notice of Funding Opportunity (NOFO) to support a limited competition renewal of the Analysis, Visualization, and Informatics Lab-space (AnVIL) program. AnVIL is a secure, cloud-based platform that enables researchers to access, share, and analyze large-scale genomic datasets without relying on local infrastructure. Currently, AnVIL hosts more than 5 petabytes of data from nearly 300,000 research participants, providing a robust environment for reproducible, cloud-native genomic research.The renewed program will continue to advance AnVIL as a community resource grounded in FAIR (Findable, Accessible, Interoperable, and Reusable) principles. Key priorities include enhancing scalability; strengthening interoperability across a federated NIH data ecosystem; and maintaining rigorous security aligned with the Research Authentication Service (RAS) and NIH controlled-access data repositories and access management systems (CADR) requirements (see NOT‑OD‑25‑159). The renewal will also support integration of emerging data types and computational tools, including infrastructure for developing and running AI-based methods and complex analysis workflows.In addition to platform development, the program will expand training and outreach to help researchers effectively use AnVIL’s multimodal datasets and reproducible analysis capabilities. By connecting secure data access, analytical tools, and workforce development, the renewed AnVIL program aims to accelerate discovery across the research lifecycle and strengthen the genomics community’s capacity for clinical and translational science.This Notice is being provided to allow potential applicants sufficient time to develop responsive applications. The NOFO is expected to be published in 2027 with an anticipated application due date in 2027. This NOFO will utilize the U54 activity code.This is a Forecast for a limited competition that will invite application(s) from eligible organization(s) to apply. Please see Eligibility Section for additional information. In accordance with NIH standard peer-review processes, the application(s) will be peer-reviewed, and only meritorious application(s) will be considered for funding.

2027-05-25

HealthArts & Culture

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Lineage tradeoffs during injury-accelerated intestinal cell differentiation

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY Barrier epithelia face continual damage from environmental insults, and successful injury repair is crucial for organismal health. A prime case study is the one-cell-thick intestinal epithelium, which forms a leakproof bar- rier between the gut lumen and the body cavity. To replace damaged cells, the intestine mobilizes stem cells to divide rapidly; to restore intestinal form and function, these new daughter cells must also differentiate rapidly. Indeed, injury-born intestinal cells acquire their mature identity twice as fast as their normal counterparts. Using the Drosophila adult intestine, we recently discovered this injury-accelerated differentiation arises through disruption of Notch-Delta lateral inhibition circuitry that normally specifies stem versus terminal fate. During injury, many newly born cells exhibit >10x faster Notch signaling speed, which propels faster intestinal differentiation to restore the breached epithelial barrier. Yet this strategy comes with risks for long-term tissue health: For stem cells, loss of Notch-Delta feedback during injury skews daughter fates toward dead-end, ter- minal:terminal outcomes, which depletes the organ’s stem cells and culminates in stem cell exhaustion. For terminal progeny, accelerated differentiation yields provisional ‘stopgap’ cells—mature cells with digestive and barrier-forming functions but altered morphology and a supercompetitor-like transcriptomic profile. Here, we will investigate how the organ copes with these two tradeoffs. We combine physiological injury of the fly gut with in vivo live imaging and cutting-edge cell lineage tracing to elucidate how these ‘side effects’ of accelerated differentiation are managed at the organ-scale for post-injury tissue homeostasis. The fly gut com- bines conserved intestinal cell lineages, fate signals, and digestive physiology with supreme experimental trac- tability: A single Notch receptor and Delta ligand, an unparalleled wealth of genetic tools, and long-term in vivo live imaging—pioneered by our lab—provide the technical bases for deep mechanistic investigation. Leveraging these strengths, in Aim 1 we will define how some, ‘escaper’ stem cells persist after injury, de- spite disrupted Notch-Delta feedback that should force all cells to differentiate. We will test if escaper stem cells inherit an intracellular Notch inhibitor, autonomously override how Notch and Delta interact, or lose con- tact with their signaling partners via injury-induced epithelial fluidization. In Aim 2, we will ascertain the time- evolution and function of stopgap cells during and after injury. We will determine their ultimate fates in the tis- sue during recovery, e.g., they may evolve into normal cells, arrest in an abnormal state, or simply be shed. We will parse these scenarios using longitudinal live imaging, whole-population analyses, and single-cell tran- scriptomics. Finally, we will examine how stopgap cells shape the tissue post-injury by ‘purging’ unfit, toxin- exposed cells during injury or by exerting selective pressure on new cells during post-injury recovery. By probing these lineage tradeoffs of accelerated cell differentiation during injury, our work will suggest new strategies to promote intestinal regeneration and combat chronic intestinal disease.

Up to $631K

2031-01-31

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Linear diribonucleotides regulation of bacterial physiology and infections

NIAID - National Institute of Allergy and Infectious Diseases

RNA degradation was thought to proceed through endonucleolytic fragmentation, followed by exo- ribonuclease trimming which generate short RNA fragments that are turned over into mononucleotides by oligoribonuclease (Orn). In the last funding period, we published data supporting that only specific enzymes (Orn, NrnA, NrnB, and NrnC) cleave diribonucleotides into monoribonucleotides, and that prokaryotic organisms need to encode at least one diribonuclease to fulfill this specific function. These results support a new perspective on RNA degradation in which the short oligoribonucleotides are processed through a sequence of discrete steps involving distinct enzymes. In addition, linear diribonucleotides appear to be biologically active molecules since we reported that mutants lacking these enzymes accumulate diribonucleotides and have altered cell growth, biofilm formation, motility, and sporulation. Here we present additional preliminary data supporting diribonucleotides as active signaling molecules in the cell including: 1. Specific enzymes act trinucleases to generate diribonucleotides, 2. RNase AM of Pseudomonas aeruginosa ∆orn is a cryptic diribonuclease, 3. Two enzymes in central metabolism are diribonucleotide- binding proteins, and 4. P. aeruginosa ∆orn has virulence defects in an animal model of catheter-associated urinary tract infection. Our past publications and preliminary data provide the scientific premise for our hypothesis that cells generate linear dinucleotides from RNA degradation and linearization of cyclic dinucleotides, which can bind target proteins to alter cell physiology and pathogenesis. To test these aims, we will perform the following specific aims: In Aim 1, we will characterize the generation and degradation of diribonucleotides by characterizing how diribonucleases and triribonucleases bind their respective substrates through molecular biology, biochemistry, and computational docking. In Aim 2, we will identify effects of dinucleotides on bacterial metabolism and physiology by characterizing the binding proteins that specifically interact with linear diribonucleotides. Building on our success of identifying cellular diribonucleotide receptors, we will screen for additional proteins from open reading libraries of P. aeruginosa and Bacillus anthracis. We will exploit the strains available to us that lack all diguanylate cyclases to reveal whether the effect of linear diribonucleotides is independent of c-di-GMP signaling. In Aim 3, we will characterize the effect of expression levels of dinucleases and the effect of dinucleotide accumulation on bacterial physiology and pathogenesis. We will develop mass spectrometry methods to detect di- and triribonucleotides. We will employ existing mutants lacking diribonucleases, including P. aeruginosa ∆orn to study the defects in chronic infection in a murine model of catheter-associated urinary tract infection. Results from these studies will advance our understanding of RNA degradation and open a new area of signaling by linear diribonucleotides with the potential to be applied to novel antibacterial strategies.

Up to $571K

2031-05-31

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LINENS

TABB TEXTILES INC

Domestic Appliances and Supplies and Consumer Electronic Products-Bedclothes and table and kitchen linen and towels-Towels-Bath towels

2027-10-31

general

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Linguistics

science_technology_and_other_research_and_developmentArts & Culture

U.S. National Science Foundation

The Linguistics Program supports basic science in the domain of human language, encompassing investigations of the grammatical properties of individual human languages, and of natural language in general. Research areas include syntax, semantics, morphology, phonetics and phonology. The program encourages projects that are interdisciplinary in methodological or theoretical perspective, and that address questions that cross disciplinary boundaries, such as (but not limited to): <ul> <li>What are the psychological processes involved in the production, perception, and comprehension of language?</li> <li>What are the computational properties of language and/or the language processor that make fluent production, incremental comprehension or rapid learning possible?</li> <li>How do the acoustic and physiological properties of speech inform our theories of natural language and/or language processing?</li> <li>What role does human neurobiology play in shaping the various grammatical properties of language?</li> <li>How does language develop in natural learning contexts across the life-span?</li> <li>What social and cultural factors underlie language variation and change?</li> </ul> Because NSF's mandate is to support basic research, the Linguistics Program does not fund research that takes as its primary goal improved clinical practice or applied policy, nor does it support work to develop or assess pedagogical methods or tools for language instruction. The Linguistics Program accepts proposals for a variety of project types: research proposals from scholars with PhDs or equivalent degrees, proposals for <a href="https://new.nsf.gov/funding/opportunities/linguistics-program-doctoral-dissertation-research">Doctoral Dissertation Research Improvement (LING-DDRI)</a> awards, and <a href="https://new.nsf.gov/funding/opportunities/faculty-early-career-development-program-career">CAREER</a> proposals. We will also consider proposals for conferences. Funding requests for conference support should be submitted in accordance with the Conference Proposals section of Chapter II of NSF's <a href="https://new.nsf.gov/policies/pappg">Proposal & Award Policies & Procedures Guide (PAPPG)</a>. NSF's Division of Behavioral and Cognitive Sciences (BCS), in partnership with the National Endowment for the Humanities and in collaboration with programs in other NSF Directorates, supports efforts to develop and advance knowledge and infrastructure that will enable the analysis of languages that are both understudied and at risk of falling out of use. In recognition of the critical relevance of these languages to understanding the range and limits of human linguistic and cultural variation, BCS accepts research and dissertation proposals in response to solicitations <a href="https://new.nsf.gov/funding/opportunities/nsf-dynamic-language-infrastructure-neh">NSF Dynamic Language Infrastructure - NEH Documenting Endangered Languages (DLI-DEL)</a> and <a href="https://new.nsf.gov/funding/opportunities/dynamic-language-infrastructure-doctoral">Dynamic Language Infrastructure - Doctoral Dissertation Research Improvement Grants (DLI-DDRI)</a>. For more information about Multidisciplinary Research and Training Opportunities, please visit the <a href="https://www.nsf.gov/div/index.jsp?div=SMA">SBE Office of Multidisciplinary Activities web site.</a>

2026-07-15

Free to search & build · $99 one-time to unlock the application pack · No subscription

Linguistics

U.S. National Science Foundation

Linguistics

2026-07-15

general

Free to search & build · $99 one-time to unlock the application pack · No subscription

Linguistics

U.S. National Science Foundation

The Linguistics Program supports basic science in the domain of human language, encompassing investigations of the grammatical properties of individual human languages, and of natural language in general. Research areas include syntax, semantics, morphology, phonetics and phonology. The program encourages projects that are interdisciplinary in methodological or theoretical perspective, and that address questions that cross disciplinary boundaries, such as (but not limited to): What are the psychological processes involved in the production, perception, and comprehension of language? What are the computational properties of language and/or the language processor that make fluent production, incremental comprehension or rapid learning possible? How do the acoustic and physiological properties of speech inform our theories of natural language and/or language processing? What role does human neurobiology play in shaping the various grammatical properties of language? How does language develop in natural learning contexts across the life-span? What social and cultural factors underlie language variation and change? Because NSF's mandate is to support basic research, the Linguistics Program does not fund research that takes as its primary goal improved clinical practice or applied policy, nor does it support work to develop or assess pedagogical methods or tools for language instruction. The Linguistics Program accepts proposals for a variety of project types: research proposals from scholars with PhDs or equivalent degrees, proposals for Doctoral Dissertation Research Improvement (LING-DDRI) awards, and CAREER proposals. We will also consider proposals for conferences. Funding requests for conference support should be submitted in accordance with the Conference Proposals section of Chapter II of NSF's Proposal & Award Policies & Procedures Guide (PAPPG). NSF's Division of Behavioral and Cognitive Sciences (BCS), in partnership with the National Endowment for the Humanities and in collaboration with programs in other NSF Directorates, supports efforts to develop and advance knowledge and infrastructure that will enable the analysis of languages that are both understudied and at risk of falling out of use. In recognition of the critical relevance of these languages to understanding the range and limits of human linguistic and cultural variation, BCS accepts research and dissertation proposals in response to solicitations NSF Dynamic Language Infrastructure - NEH Documenting Endangered Languages (DLI-DEL) and Dynamic Language Infrastructure - Doctoral Dissertation Research Improvement Grants (DLI-DDRI). For more information about Multidisciplinary Research and Training Opportunities, please visit the SBE Office of Multidisciplinary Activities web site.

2026-07-15

sciencetechnology

Free to search & build · $99 one-time to unlock the application pack · No subscription

Linguistics Program - Doctoral Dissertation Research Improvement Grants

U.S. National Science Foundation

rolling

sciencetechnology

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Linking physiology, computation and circuitry in the primate visual cortex

NEI - National Eye Institute

PROJECT SUMMARY The aim of this proposal is to determine the biological underpinnings of canonical computations in the brain. The focus will be on how these computations manifest in primate visual system, which is the classical system for identifying such transformations of information. Canonical computations are fundamental processing patterns that underlie a wide range of neural functions, impacting perception and cognition across hierarchical brain networks. However, there are large families of possible biological circuits that could implement these computations and, likewise, vastly different computations can be implemented with the same or very similar neural circuitry. What is needed to advance our understanding of these computations in the brain is a way to bridge the gap between physiology, computation and circuitry in a tractable, generalizable model living system. Marmoset early visual areas V1 and V2 are the perfect testbed to develop models of cortico-cortical computations and circuits, some of which will generalize to the rest of the visual system and to hierarchical transformations of information throughout the primate neocortex. An exhaustive dataset of simultaneous V1 and V2 neural responses with high density electrophysiology and calcium imaging will be collected in combination with perturbations using virally mediated opto- and chemo-genetic tools to test models of a canonical interareal circuit. In contrast to the mouse model, where these tools have largely been developed and implemented, the marmoset has prototypical primate neural circuits closely related to our own, but in a simpler and more accessible brain than that of larger primates. The training aims of this proposal support the development of the analysis and genetic tools that are required to understand the transformation of information between V1 and V2. These support an independent research phase, to dissect the circuits involved in interareal transformations and extend the analysis to additional stages of the visual hierarchy. The overall goal of the project is to understand the transformation of information between areas in the visual system ultimately to arrive at a canonical model for cortico-cortical computation and circuitry across the brain.

Up to $132K

2028-04-30

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Linking Single-Cell Transcriptomic, Morphological, and Temporal Signatures of Vulnerability in Neurodegeneration

NINDS - National Institute of Neurological Disorders and Stroke

Neurodegeneration involves complex cellular phenotypes and molecular changes that vary widely among the cells of the nervous system. Current methodologies permit either detailed molecular profiling (e.g., single-cell transcriptomics) or functional phenotyping (e.g., live imaging of neuronal activity), but not both in the same cells. Thus, it is difficult to directly link a neuron's functional state or fate with its gene expression profile. To address this limitation, we developed an innovative technology, VISTA-FISH (Video Imaging with Spatial- Temporal Analysis by FISH), that couples prospective live-cell imaging with high-resolution spatial transcriptomic profiling of the same cells. This approach enables in situ comparisons of gene expression in neurons that exhibit divergent behaviors or outcomes. Using VISTA-FISH, we will profile iPS-derived human neurons to link single-cell gene expression, morphology, and temporal phenotypes to study molecular pathways driving resilience as well as susceptibility. After exposing neurons carrying TDP43 and C9orf72 mutations to a stimulus inducing TDP43 aggregation, we will jointly record TDP43 localization and neuron activity using live-cell microscopy, then measure single-cell gene expression of the same cells (Aim 1). We will also combine live-cell measurements of TDP43 half-life with CRISPR screening and single-cell gene expression (Aim 2). These rich datasets will enable us to determine transcriptomic changes associated with differences in protein aggregation, protein synthesis, and protein degradation in individual cells, providing an unprecedented molecular perspective on factors responsible for vulnerability and resilience to neurodegeneration.

Up to $602K

2031-03-31

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Linking temporal context reinstatement to temporal memory interference

NINDS - National Institute of Neurological Disorders and Stroke

Project Summary/Abstract The ability to remember when events occurred in time is not only a defining feature of episodic memory, but it is an essential feature for adaptively using memory to guide behavior. However, temporal memory is particularly prone to interference due to the fact that many of the people, locations, objects, and actions that feature in our memories tend to repeat or re-occur across time. For example, remembering when you last took a medication is complicated by interference from other memories of taking that same medication at other points in time. Thus, understanding how temporal memories are protected against interference represents an important question that is fundamental to theories of memory. Moreover, it is a topic that is highly relevant to real-world forgetting—particularly because susceptibility to temporal memory interference is often exacerbated with aging and neurodegenerative disease. Despite the importance of temporal memory, the mechanisms that protect against temporal memory interference remain poorly understood. Leading computational models of memory argue that when a stimulus re-occurs (e.g., re-watching a movie) this triggers a reinstatement of the ‘temporal context’ in which it previously occurred. In the proposed research, we will develop novel fMRI methods to measure temporal context reinstatement and to test how/whether temporal context reinstatement influences temporal memory. We will consider not only whether reinstatement influences memory for when events previously occurred, but also whether reinstatement influences temporal memory for ongoing events. Additionally, we will characterize temporal memory not only in terms of the accuracy of temporal memory estimates (the degree of error), but also potential biases in temporal memory estimates (the tendency to remember events as closer or farther apart than they actually were). Finally, motivated by recent work from human and rodent studies implicating medial temporal lobe regions in temporal processing and temporal memory, we will use high-resolution imaging to establish how subregions of the medial temporal lobe—including hippocampal subfields—contribute to temporal context reinstatement and protect against temporal memory interference. The expected outcomes of the proposed research are (1) innovative new fMRI methods for measuring temporal context reinstatement, (2) an understanding of the extent to which temporal context reinstatement influences/protects temporal memories, and (3) new insight into how subregions of the medial temporal lobe system contribute to temporal context reinstatement and temporal memory.

Up to $227K

2027-12-31

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Lions Clubs International Foundation Community Service Grants

vision healthhunger reliefenvironment+2

Lions Clubs International Foundation

Supports vision health, hunger relief, environmental programs, childhood cancer, and disaster relief through Lions clubs worldwide.

$5K – $250K

Rolling

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Lipid Degradation in Human Milk and Preterm Gastrointestinal Outcomes

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

PROJECT SUMMARY Human milk is a vital bioactive substance and a significant driver of health outcomes for preterm infants. Milk constituents can degrade in storage, and long-chain polyunsaturated fatty acids are most susceptible to chemical instability. The products of lipid degradation and lipid oxidation are widely implicated in various diseases; however, their impact on the intestinal outcomes of preterm infants is poorly understood. This presents a significant opportunity to enhance our understanding of how milk storage may impact the risk of life-threatening gastrointestinal diseases, particularly necrotizing enterocolitis (NEC). Two primary aims of this proposal are (1) to evaluate the role of fatty acid-protein complex (FAPC) formation in donor milk in driving preterm intestinal stress and mitochondrial toxicity, and (2) to determine whether secondary lipid oxidation products in human milk are associated with clinical NEC and promote intestinal injury in human enteroids. Tissue-derived enteroids will be used to investigate how mitochondrial stress and barrier integrity are affected by lipid metabolites present in human milk. This proposal will integrate a comprehensive set of prospective patient data with human milk samples collected in the Medical University of South Carolina Pediatric Biorepository. The study will employ advanced laboratory- based models of preterm and neonatal enteroids. The degree of lipid degradation in banked donor human milk will be quantified using LC-MS, and Fourier-transform MS will be evaluated as a novel approach for detecting fatty-acid protein complexes. End points of mitochondrial dysfunction in preterm enteroids will be measured after exposure to products of lipid oxidation generated in stored milk. Lastly, new approaches to milk storage could inform new recommendations that would sustain its highest possible quality. Dr. Katherine Chetta’s long-term vision is to become a productive, independent physician-scientist and an expert in the field of human milk lipids and preterm gastrointestinal health. Receiving a Mentored Patient-Oriented Research Career Development Award allows her to investigate novel pathways for human milk research at the Medical University of South Carolina (MUSC). Under the guidance of an expert team of mentors, she will acquire advanced laboratory-based skills in milk analysis and preterm translational models, preparing her for launching an independent laboratory. The proposed K23 award would facilitate Dr. Chetta’s ultimate career goal of optimizing human milk and preterm gastrointestinal health, thereby benefiting critically ill and preterm infants.

Up to $183K

2029-05-31

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Lipid Droplets

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY Lipid Droplets (LDs) are rapidly emerging as critical adaptive organelles at the nexus of lipid metabolism and human disease. The 10th FASEB Summer Research Conference on "Lipid Droplets" will delve into this rapidly evolving field. As the primary cellular lipid storage organelles, LDs serve as vital hubs of lipid metabolism, influencing energy storage, lipid signaling, membrane biogenesis, and lipotoxicity. Pathological LD accumulation is a hallmark of metabolic diseases including obesity, insulin resistance, diabetes, fatty liver disease, lipodystrophy, cancers, cardiovascular diseases, and neurodegeneration. The growing prevalence of metabolic disorders in the United States underscores urgency to mechanistically understand the molecular underpinnings of LD formation, growth, movement, and turnover. Understanding LD biology promises novel therapeutics and is thus of high interest to scientists in academic, pharmaceutical, and biotechnology sectors. This conference will take place from July 26 to 30, 2026, in Scottsdale, AZ, USA. It will co-locate with the FASEB SRC Phospholipids conference, and include three keynote addresses from lipid metabolism leaders: Dr. Hugo Bellen (Baylor College of Medicine, HHMI), Dr. Elina Ikonen (University of Helsinki), and Dr. Bruno Anthonny (CNRS). As the longest-running meeting solely focused on LD biology, it will feature a multi- disciplinary speaker line-up focused on leading-edge research in basic and clinical science. The conference format comprises eight sessions featuring talks by invited speakers, 15 short talks selected from submitted abstracts, two poster sessions (together with the FASEB SRC Phospholipid conference), a Career-Oriented Workshop, and Meet-the-Experts sessions. Its trainee-focused environment has been carefully crafted to foster interactions between trainees, early career investigators, and established researchers. Scientific sessions will span the entire spectrum of LD biology. Distinguished researchers will deliver talks spanning many approaches (biophysics, genetics, biochemistry, cell biology, physiology) and cutting-edge technologies (chemical biology tools, lipidomics, new imaging approaches) in a range of model systems (cultured cells, Drosophila, yeast, C. elegans, mice, humans). A primary aim of this conference is to nurture and empower the next generation of scientists. To that end, we seek funding to support the participation of 15 graduate students, postdoctoral fellows, and early career investigators. The conference's informal and trainee-oriented setting will provide numerous opportunities for planned and spontaneous informal interactions, affording young investigators the chance to present their work, obtain valuable feedback from leaders in the field, and receive career guidance. In closing, this conference stands as the pioneering international gathering dedicated exclusively to lipid droplet biology and its profound relevance to human diseases. It continues to serve as a unique and memorable forum for researchers to exchange ideas and share groundbreaking results.

Up to $25K

2027-02-28

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Lipid peroxidation- and pyroptosis-induced tissue factor activation in pathogen-induced blood coagulation

NHLBI - National Heart Lung and Blood Institute

Tissue factor (TF), the primary initiator of the blood coagulation cascade, is carefully regulated to prevent aberrant coagulation activation. However, pathological conditions including bacterial and viral infection induce intravascular TF expression and lead to thrombosis. As TF-induced thrombosis is a major cause of acute myocardial infarction, ischemic stroke, and pulmonary embolism, improved understanding of the mechanisms of pathological TF activation may lead to new therapeutic targets. Pyroptosis, a form of inflammatory cell death, drives TF-mediated intravascular coagulation activation in bacterial sepsis. Emerging studies also implicate inflammasome activation in viral infections, but its role in TF activation is unknown. Our preliminary studies demonstrate that ORF3A, an accessory viral protein induce TF activation in a phosphatidylserine (PS)-dependent mechanism that requires TMEM16F, similar to PS-dependent TF activation in pyroptosis. In Aim 1, my lab will investigate the underlying mechanisms that govern ORF3a-induced TF activation emphasizing the key roles of programmed-cell death. Lipid peroxidation and its highly reactive end products such as 4-hydroxy-2-nonenal (HNE) are involved in various forms of programmed cell death including pyroptosis. However, the role of HNE, the most stable and toxic reactive aldehyde produced during lipid peroxidation, in pyroptosis-associated TF and coagulation activation is not known. Our preliminary data showed that HNE induces PS-dependent TF activation in LPS-primed macrophages and causes intravascular coagulation activation in mice. However, the complete mechanism by which HNE induces PS externalization and TF activation is not known. In Aim 2, my lab will use chemical and genetic approaches to investigate whether HNE-induced TF activation and intravascular coagulation activation is mediated through programmed cell death. Although lipid peroxidation plays a central role in cell death and coagulation activation in bacterial sepsis, a therapeutically targetable enzyme responsible for the unbridled lipid peroxidation and generation of pathological levels of reactive radicals such as HNE is not known. In Aim 3, my lab will use genetically modified mice deficient in lipid peroxidation and HNE formation to investigate TF-dependent pathologic coagulation activation and thrombosis during sepsis. A successful completion of these studies will help delineate a common pathway involved in pathologic TF activation across varied pathogenic infections and will also help identify a specific therapeutically targetable enzyme to attenuate TF activation in disease.

Up to $249K

2029-04-30