Grants

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY/ABSTRACT Acute kidney injury (AKI) has a rising incidence among hospitalized patients and the risk for progression to chronic kidney disease (CKD) has been established in both pre-clinical and clinical studies; however, there is still a knowledge gap on the molecular mechanisms driving the AKI to CKD transition. We previously identified Foxm1, a transcription factor considered to be a master regulator of the cell cycle, as having a role in tubular epithelial proliferation in a mouse model of acute ischemic renal injury, Subsequent studies using genetic deletion mouse models demonstrated that Foxm1 is involved in proximal tubular epithelial proliferation after injury in vivo. Furthermore, impaired tubular proliferation due to Foxm1 deletion led to an early AKl-to-CKD transition phenotype highlighting its pro-repair role; however, the exact mechanism for the profibrotic effect of Foxm1 deletion is unclear. Our recent in vitro work has identified a novel Foxm1 target mediating proliferation - the cyclin family membercyclin F (CCNF), CCNF is a gene with a role in cell cycle progression and genome stability, Induction of cell cycle arrest and genome instability have been described to promote the development of cellular senescence. In preliminary studies, we observed that expression of cell senescence markers and components of the senescence secretory phenotype (SASP) correlate with repression of Foxm1 induction after injury suggesting that Foxm1 deletion may be driving increased cellular senescence. This let us to hypothesize that (1) Tubular epithelial cells that failed to repair undergo cellular senescence which drives the AKI to CKD transition and (2) this process is mediated by downregulation of the Foxm1-CCNF axis inducing cell cycle arrest and genome instability, In Aim 1, we will characterize how Foxm1 repression during tubular epithelial repair leads to cellular senescence and in turn transition to CKD. In Aim 2, we will determine if CCNF repression triggers the transition to cellular senescence and identify potential downstream pathways, In this application we aim to understand how alterations in the pro-repair effects of Foxm1 lead to unsuccessful repair and development of cellular senescence with the goal of identifying areas for therapeutic interventions through senolytics (cell senescence removal) or senomorphics (suppress the SASP),

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY/ABSTRACT Benign prostatic hyperplasia (BPH) and associated lower urinary tract symptoms (LUTS) is a prevalent condition among aging men, affecting ninety percent of all men above the age of eighty years. The causes of BPH/LUTS are considered multifactorial although it is known that aging is the number one risk factor for development and progression of disease. Despite initial effectiveness, current medical management strategies that target smooth muscle dysfunction or prostatic proliferations often fail to effectively manage disease progression, leading patients to seek out invasive surgical interventions. A key factor hypothesized to contribute to BPH/LUTS progression is prostatic fibrosis, which current therapies do not address. Age mediated cellular senescence, defined as a stable and irreversible cell-cycle arrest, has been implicated in the dysregulation of prostate tissue homeostasis. I hypothesize that age-mediated cellular senescence within the prostate drives prostatic fibrosis and therefore contributes to the development of lower urinary tract dysfunction (LUTD) and BPH. Our study aims to determine the role of senescent cells in BPH/LUTS pathogenesis and evaluate the therapeutic potential of senescent cell elimination. I aim to evaluate this hypothesis using clinical human prostate tissues and mouse models for BPH/LUTS. Specifically, I will investigate whether the degree of lower urinary tract senescence correlates with dysfunction and if targeting p16-positive senescent cells can decrease prostate fibrosis and improve urinary health. Additionally, I will examine the relationship between senescent cells and prostatic fibrosis in human BPH tissues and assess the impact of pharmacologically eliminating senescent cells using a clinically translatable senolytic dasatinib and quercetin (D+Q) in aged mice. This research will provide insights into the role of cellular senescence in BPH/LUTS and explore novel therapeutic approaches to improve patient outcomes. The extensive resources at the University of Wisconsin School of Medicine and Public Health create an optimal setting for the successful execution of this proposed work. Completing this study will foster the development of crucial experimental, mentorship, communication, and clinical skills, facilitating a smooth transition to a career as an independent researcher and surgeon-scientist.

NIAMS - National Institute of Arthritis and Musculoskeletal and Skin Diseases

Summary Osteoarthritis (OA) is influenced by factors like joint injury, age, and gender. Chronic pain is the primary debilitating symptom, and current treatments are ineffective and do not reduce disease progression. Understanding OA and developing therapies is challenging because pain does not always correlate with joint damage. Targeting mechanisms that regulate joint tissue integrity and inflammation simultaneously may be necessary to alleviate pain and limit further physical deterioration. Our research identified the role of IRE1α- XBP1 in inflammatory pain and showed that leukocyte-specific IRE1α deficiency reduced pain and inflammatory mediators. We have uncovered that XBP1 transactivates NUPR1, which, when expressed in chondrocytes, leads to apoptosis and cartilage degradation. Furthermore, our studies demonstrate that global deletion of NUPR1 reduced OA pain and structural changes in mice, suggesting that the IRE1α-XBP1-NUPR1 axis regulates inflammation and tissue damage in OA. Thus, we hypothesize that IRE1α-XBP1-NUPR1 drives OA by promoting inflammatory programs in synovial immune cells while fostering joint cartilage damage via catabolic changes in chondrocytes. We will implement our plan through these specific aims: 1. Define how IRE1α-XBP1-NUPR1 signaling in immune cells and chondrocytes differentially contributes to synovial inflammation, cartilage damage, and OA pain. Two knee OA models (an injured model and an aging model) will be used in conditional knockout (cKO) mice lacking IRE1 or NUPR1 exclusively in leukocytes (Vavcre Ern1fl/fl) or chondrocytes (Col2a1cre Ern1fl/fl). Pain related behaviors and structural and molecular changes in the knee will be evaluated over time. 2. Determine how the IRE1α-XBP1-NUPR1 axis programming affects immune cell and chondrocyte function to drive OA joint structural damage, inflammation, and sensory neuron hyperactivity. We will use transgenic reporter mice that exhibit Venus-green fluorescent protein expression upon IRE1α-XBP1 activation to define the anatomical, cellular, and temporal IRE1α activation in the injury-link OA knee and study the functional phenotype of FACS sorted immune cells based on IRE1α activation. Then, we will discern how intrinsic leukocyte or chondrocyte IRE1α (cKO) sculpts the transcriptomic landscape and pathological microenvironment of the OA joint, and how IRE1α dictates leukocyte-chondrocyte interactions via single cell RNA sequencing and interactome bioinformatic analyses. 3. Test the translational hypothesis that inhibiting IRE1α or NUPR1 prevents or limits the progression of OA. We will use pharmacological blockers of IRE1α or NUPR1 to prevent or reverse OA-related pain behaviors and joint structural damage. Our project will establish IRE1α-XBP1-NUPR1 axis as a disease modifying target that would reduce pain and enhance joint functionality. Our unique transgenic mouse lines enable precise dissection of this specific OA molecular mechanism. Our multidisciplinary team is uniquely equipped to successfully complete these studies as we combine expertise in neuroimmunology and pain, cartilage and chondrocyte biology, and genomics coupled with advanced bioinformatic analytical tools.

NIGMS - National Institute of General Medical Sciences

PROJECT SUMMARY/ABSTRACT: Sepsis results from a dysregulated host response to infection leading to life-threatening organ dysfunction. It is a complex and dynamic disease process, and a leading cause of morbidity and mortality in intensive care units (ICUs). Due to the therapeutic challenges of patients with sepsis, and the fact that management remains predominantly supportive, there is an undeniable need to develop new treatment strategies for sepsis. New advances being explored include cell-based therapies. For more than 25 years my laboratory has explored the pathobiology of sepsis, and related organ injuries, including the lung. Our approach is to investigate mechanisms of disease, starting at the cellular level in vitro and translating these findings into models of disease ex vivo and in vivo. To complement our work further in sepsis, with an interest in therapy, we became interested in stem/stromal cells. My laboratory has explored the use of mesenchymal stem/stromal cells (MSCs) for therapeutic intervention in pre-clinical models of sepsis and lung injury. We investigate mechanisms responsible for the biological activity of MSCs, including paracrine actions via their conditioned medium and the impact of MSC-derived extracellular vesicles (EVs) and their cargo (miRNAs). To advance our understanding of cellular therapy for sepsis, we recently began to explore a new source of cells – placenta-derived trophoblast stem cells (TSCs). Our laboratory was the first to isolate murine (m) TSCs, using CD117 as a cell surface marker of stem/progenitor cells. Beyond paracrine actions, these cells can engraft and differentiate into parenchymal cells. We now propose to advance our investigation of TSCs harvested from human(h) term placentas. hMSCs are immune evasive, and hTSCs are immune privileged, allowing the use of both cells for allogeneic therapy. We will investigate hMSCs and hTSCs to modify the pathobiology of sepsis and provide insight into the immune response to eradicate microbes, resolve inflammation, and decrease organ injury along with promoting repair. Sepsis and organ injury, such as acute respiratory distress syndrome (ARDS), are very heterogeneous clinical processes, thus targeting a specific biological pathway is challenging. We propose that viable therapeutic cells will sense the underlying septic environment, and respond accordingly with varied paracrine actions. Plasma and immune cells from patients with sepsis ± ARDS, compared with ICU control (non-infected) patients, will allow us to explore a personalized approach using hMSCs and hTSCs. Moreover, due to differences that exist between human and mouse lungs, we propose to evaluate the actions of hMSC and hTSCs using human lung organoids and precision-cut lung slices (PSLS) as human models of lung/alveolar injury, and transcriptomic approaches to identify pathways critical for disease modification. Thus, our vision is to advance the insight into therapies for sepsis using hMSCs and hTSC, and that using human models of disease in vitro, ex vivo, and with confirmation in a pre-clinical model of pneumosepsis will provide insight into critical sepsis pathways and advance our approach to the therapy of sepsis and ARDS.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

Project Summary Autosomal Dominant Polycystic Kidney Disease (ADPKD) is incurable, and cellular systems for modeling the genetics of cystogenesis are needed to understand the underlying pathways and to design preventatives. Mice do not faithfully recapitulate natural ADPKD, presenting a major limitation to cystogenesis research. In humans, cysts are formed when the PKD1 gene product, polycystin-1, is disrupted. Most cysts originate from a somatic “second hit” inactivation of one PKD1 allele, which joins the inherited pathogenic allele to result in biallelic inactivation. It happens hundreds of times in human ADPKD, but in mice Pkd1 heterozygotes do not form cysts and the gene escapes mutation. We discovered why, and will use that information here to create novel cellular tools for ADPKD research. We find that a defining characteristic of human PKD1 is an unusual capacity to form guanine-quadruplex (G4) DNA structures. G4 DNA is found throughout the genome where it helps regulate gene expression, but it is unusually abundant in human PKD1. G4 DNA is highly stable in the cell, concentrated in the 5’ region of genes, and is normally resolved by G4-specific helicases to prevent polymerase stalling and DNA breaks. G4-stabilizing ligands, reporter assays, and direct visualization in living cells has validated the contributions of G4 DNA to cell physiology as well as documented the propensity of the structure to increase locus-specific mutagenesis. Human PKD1 harbors ~10-times more G4 DNA than mouse Pkd1, and we observed G4 formation in human PKD1 by chromatin immunoprecipitation. Incubation of human cells with a G4-stabilizing ligand resulted in DNA breaks in PKD1, and lowered its expression. G4 DNA does not measurably form in mouse Pkd1 or cause DNA breaks in the gene. Since mutagenic inactivation of human PKD1 causes cysts and G4 DNA provokes breaks in the gene, G4 DNA regulates cystogenesis. Based on that premise, we will develop pluripotent stem cells altered for PKD1 G4 content, thereby creating a unique tool for cystogenesis research. In Aim 1 we will transfer two blocks of human PKD1 G4 repeats to mouse Pkd1 in induced pluripotent stem cells, thereby humanizing the murine ortholog in a cellular system capable of renal cell development. In Aim 2, we will delete two G4-rich regions (introns 21 and 22) from human PKD1 in pluripotent stem cells and in HEK293T, providing two novel cell-based reagents for studying the impact of G4 DNA on polycystin-1 activity in a genetic background amenable to cystogenesis studies. Following their validation as G4-modified PKD1 cell models, reagents will be made freely available for studies on ADPKD mechanisms and potential therapeutic interventions.

Celtic Arts Foundation

Celtic Arts Foundation is an active grantmaking foundation based in Mount Vernon, WA. Focus: arts. Contact the foundation directly for current funding opportunities.

Bristol

Cemeteries Hazardous Tree Removal

Salisbury

Cemetery Restoration

Centennial School Foundation

Centennial School Foundation is an active grantmaking foundation based in Utica, NE. Focus: general. Contact the foundation directly for current funding opportunities.

National Park Service

The overall mission of the NPS Centennial Volunteer Ambassador Program is to support park units service-wide in expanding volunteerism, service-learning, and community engagement programs and activities to new audiences and communities. The program will allow the NPS to help develop the next generation of lifelong conservation stewards and ensure a skilled and diverse workforce pipeline, through work & training opportunities for young adults and veterans. The program is also designed to inspire young adults and veterans (18-35 years old) from diverse backgrounds who are service focused to aspire for careers of conservation stewardship through exposure to the many difference career and leadership developmental opportunities. NPS will provide the necessary training, career development and education so that program participants can be effective and supported in their role. The Centennial Volunteer Ambassador Program will help to build a pathway which lead to a career with the NPS and/or will assist in creating the next generation of conservation stewards. SCA will provide support for 115 Centennial Volunteer Ambassadors through recruitment, enrollment, housing, transportation, training, uniform/gear; background check, Risk Management, FICA, and program support.

Young Men's and Young Women's Hebrew Association of Washington Heights and Inwood

Aging

NIGMS - National Institute of General Medical Sciences

Montana State University (MSU) is the alma mater of Maurice Hilleman, the most prolific vaccine scientist of the 20th century. The Hilleman legacy is important to MSU and a point of pride in the state of Montana. Beyond the Hilleman Scholars program and the Hilleman Research Symposium, MSU prioritizes “consequential” biomedical research aimed at understanding the molecular basis of disease. This research is supported by a BSL-3 (select agent capable) laboratory, a large animal BSL-2 facility, the only contemporary cryo-electron microscope capable of high-resolution structure determination the region, state of the art confocal and chemical imaging labs, and new investments in a cell analysis core. This existing infrastructure helps support the long-term goal of this Phase 1 Center of Biomedical Research Excellence (COBRE) to establish a sustainable Center for Advanced Molecular Pathogenesis (CAMP) that fosters recruitment, development, and retention of investigators who share a common interest in translating new discoveries in pathogenesis into new treatments, vaccines, and cures. The theme of this application is intended to be broad enough to cultivate and maintain a pipeline of new faculty with diverse model systems, techniques, and scientific perspectives, while maintaining a unified research goal that focuses on understanding mechanisms and developing treatments for disease. Significantly, this application takes advantage of a talented pool of COBRE-eligible investigators in three departments from two Montana campuses and anticipates the recruitment of additional cohorts of early-stage investigators that will benefit from professional mentoring, instrumentation, and infrastructure essential to advancing biomedical excellence at Montana State University. To achieve this long-term goal, we propose three specific aims: 1) Recruit, develop, and retain a critical mass of investigators necessary to sustain a rigorous, productive, and merit-based research Center focused on Advance Molecular Pathogenesis (CAMP), 2) Improve capacities to translate basic research discoveries into tangible benefits for individuals and society, and 3) Establish core facilities that advance the aims of early-stage investigators, and simultaneously expands the biomedical research infrastructure in Montana and the surrounding IDeA-eligible states. To accomplish these aims, we propose three initial research projects, supported by two cores: The Administrative Core and the Advanced Biological Imaging and Cell Analysis Core. The rigor and feasibility of this application is enhanced by the leadership team (which includes two former COBRE investigators), the prior training and track record of our Research Project Leaders, tailormade mentorship teams, the research infrastructure supported by this award, and active engagement with world-renowned members of our advisory committee. Success of the current cohort will create a syphon, pulling new investigators into a high-priority career development program, thereby building a critical mass of investigators with the necessary momentum to sustain a unified research Center that focuses on understanding mechanisms and developing treatments for disease.

Regional Council Capital Fund - RC5

Center for Advanced Technology Capital

NCCIH - National Center for Complementary and Integrative Health

COMMUNITY ENGAGEMENT & OUTREACH CORE – PROJECT SUMMARY / ABSTRACT The goal of the Community Engagement & Outreach (CEO) Core is to maximize stakeholder engagement for the Neuro-PRECISE Center, including researchers, clinicians, students, the public, and, importantly, consumers of rehabilitation services and their care partners and support organizations (people with lived experience, PWLE). To have a significant impact, the Neuro-PRECISE Center must substantially integrate the voice and expertise of PWLE across all levels of the center (i.e., leadership, advisory committees, administration, research and resource cores, etc.), as well as disseminate critical research findings across the domain of rehabilitation research and to a national audience. Similarly, the CEO Core will work diligently to communicate and collaborate with other funded Medical Rehabilitation Research Centers (MRRCs) and the NIH/NICHD National Center for Medical Rehabilitation Research (NCMRR) to materially contribute to a national network that is greater than the sum of any single P50 award. The CEO Core aims, goals, and approach will be guided by NIH and National Academy of Medicine reports. The Core’s specific aims are to: 1) Engage the wider stakeholder community, especially People with Lived Experience. Engaging community stakeholders to ensure their voices permeate all levels of Center programming and planning is fundamental to realizing the vision of precision neurorehabilitation in a way that is meaningful and impactful for those we serve and with whom we partner. 2) Engage the neurorehabilitation research scientific community. The CEO Core will develop, implement, and continually enhance a catalog of services and tools geared towards the wider neurorehabilitation research community that includes ongoing quarterly webinars, high-quality trainings focused on precision neurorehabilitation both locally and as satellite symposia at national conferences, and collaborative opportunities with other funded MRRCs. 3) Develop and continually enhance the Neuro-PRECISE Center outreach initiatives, communication platforms, and website. Bi-directional communication is critical to the success of an effective research center – both for sharing important research findings and building collaborative research partnerships across the field of neurorehabilitation, and for keeping abreast of the needs and desires of the Center’s multiple stakeholders to drive the science in a direction that benefits everyone. Partnerships developed through open, bidirectional communication across a cadre of vested individuals who appreciate, and value different perspectives, expertise, and experiences are needed to solve complex problems. Including PWLE throughout Center components will allow PN scientists to better understand the needs of those living with disabilities and for continual improvement of research efforts.

Senior Center of West Seattle

We have been serving the community for 52 years and through a strategic planning process, we identified a need to expand our offerings. We're planning to do this through our Center for Aging Well model where we provide programming within our current building in the Alaska Junction as well as expanding to Delridge, Arbor Heights, Morgan Junction, and Roxbury. We will update our brand image and work we do by hiring a communications consultant and graphic designer to help us with our name change. We also need a new website and we're planning to have a mural painted on the exterior of our Senior Center building.

NIAAA - National Institute on Alcohol Abuse and Alcoholism

Unhealthy alcohol use plays an important role in perpetuating HIV transmission and exacerbating HIV-associated comorbidity. Prior research has often been hampered by the reliance on self-reported alcohol use, which can be biased and inconsistent. Alcohol biomarkers can provide objective and comparable alcohol measurements for behavioral and translational alcohol and HIV research. However, research is needed to determine how to use alcohol biomarkers as intervention components to provide objective feedback to motivate behavior change, and to determine alcohol biomarker cutoffs that predict worse health outcomes for people with HIV. Engaging persons most affected by alcohol use and HIV is key to understanding the potential impact of new research innovations on the lives of those with and at risk for HIV. There is also a need to train new researchers. We propose to establish the Center for Alcohol/HIV Innovations and Biomarker Research (CALIBER), a comprehensive program of research, training, and dissemination in partnership with those affected to (1) reduce the harmful effects of alcohol use on HIV prevention and HIV-associated comorbidities, (2) advance innovations in alcohol measurement, and (3) train the next generation of alcohol/HIV investigators. CALIBER will leverage expertise in alcohol/HIV biomarker, behavioral, and translational research with the extensive data, specimens, and infrastructure of the Multicenter AIDS Cohort Study (MACS) / Women's Interagency HIV Study (WIHS) Combined Cohort Study (MWCCS), which began testing for alcohol biomarkers in 2021. CALIBER will support three projects to address gaps in alcohol-associated HIV prevention and health comorbidity. Project 1 will develop and pilot test a motivational interviewing–based intervention that incorporates biomarker feedback to reduce alcohol use and increase uptake of HIV pre-exposure prophylaxis among couples at high risk for HIV. Project 2 will adapt and test a combined brief alcohol and expressive writing intervention to reduce traumatic stress and alcohol use among women living with HIV who are recruited from the MWCCS. Both projects will be conducted remotely (phone and online) to maximize scalability. Project 3 will examine the contribution of HIV and unhealthy alcohol use to steatotic liver disease in adults with and without HIV and the role of host genomics and gut microbiome, leveraging alcohol biomarker, historical self- report, and noninvasive liver imaging for ~3000 MWCCS participants. In addition, the CALIBER Pilot Core will train, mentor, and provide pilot funding for early-stage investigators, to conduct impactful alcohol/HIV research. The Dissemination and Community Engagement Core will translate research findings into sustainable solutions for individuals affected by HIV and unhealthy alcohol use. An Administrative Core will provide oversight and administrative, budgetary, resource, and scientific enrichment support to the other cores and projects and enable CALIBER to meet its goals.

NIAID - National Institute of Allergy and Infectious Diseases

Summary The transformative advancements in cell and gene therapy have significantly enhanced our understanding and treatment of congenital diseases and regenerative medicine. As we approach the 10th annual Center for Definitive and Curative Medicine (CDCM) symposium, scheduled for March 30-31, 2026, at Stanford University's Li Ka Shing Learning and Knowledge Center, we seek financial support to facilitate this pivotal event. This symposium will serve as a platform for scientific discourse on the latest discoveries and developments in the field, inviting participation from experts and trainees across academia, non-profits, government, and industry. The two-day event will focus on the theme “Past, Present, and Future of Cell and Gene Therapy,” addressing critical challenges in translating laboratory discoveries into clinical applications. Day 1 will feature a Clinical Trial Bootcamp, workshops on relevant topics, a poster session for early- stage investigators, and an evening networking event. Day 2 will showcase luminary speakers discussing breakthroughs in lentiviral and AAV gene therapy, CAR-T, gene editing, regenerative medicine, and hematopoietic stem cell transplantation. Specific aims of the symposium include: (1) elucidating the bench-to-bedside journey through real-world case studies presented by the Stanford CIRM-funded Alpha Clinic; (2) providing a platform for graduate students and early-career researchers to present their findings; (3) facilitating workshops that address community engagement in clinical trials, the role of Artificial Intelligence in healthcare, and career opportunities in health sciences; and (4) fostering collaboration through platform sessions that expose participants to emerging research areas. This symposium has been a cornerstone of the Cell and Gene Therapy Community for the past nine years, celebrating past achievements while catalyzing future innovations. The 2026 meeting promises to be a significant milestone, driving forward the dialogue and collaboration necessary to tackle the complexities of cell and gene therapy and improve patient outcomes.

Economic Development Initiatives 16-17

Center for Economic Growth Working Capital

NYS Department of Corrections and Community Supervision

The CEO Neighborhood Work Project (NWP) provides a vocational training program that includes transitional employment for releasees.

NYS Department of Corrections and Community Supervision

The Vocational Development Program (VDP) provides job readiness activities (such as job coaching, job development and job placement) to releasees in order to prepare these individuals for employment searches and improve their employability. The VDP also provides enhanced services to releasees including an OSHA Introductory Course, several short-term certificate-based trainings and supportive services such as work supplies and financial literacy training.

National Institutes of Health

Center for Inherited Disease Research (CIDR) High Throughput Sequencing and Genotyping Resource Access (X01 Clinical Trial Not Allowed)

NIGMS - National Institute of General Medical Sciences

Biomedical problems are innately complex, and their solutions require input from many fields. Many centers focus on a single disease or organ system. By contrast, the Center for Modeling Complex Interactions focuses on an approach that can address many biomedical problems: team-based, interdisciplinary research centered around modeling. Our goal is to support and facilitate biomedical discovery by integrating modeling into interdisciplinary research. Modeling improves research at all stages, from hypothesis formulation and experimental design to analysis and interpretation, providing a unifying language that highlights commonalities and uncovers connections between problems. Formalization of ideas into this unifying language also improves rigor and reproducibility. We define modeling broadly to include everything from deterministic and stochastic mathematical approaches to physical and computational models of three-dimensional objects, to agent-based and machine learning approaches. We seek to support modelers by increasing their numbers, and by giving them opportunities to play productive roles in interdisciplinary teams. We also seek to support empiricists by giving them access to relevant modeling expertise, and by creating a community and a culture to facilitate interdisciplinary research. In Phase 1, the Center for Modeling Complex Interactions created the intellectual, cultural, and physical environment to promote team-based, interdisciplinary research. In Phase 2, we built on that foundation and created an even stronger interdisciplinary culture to foster collaboration among people who might otherwise never connect, and by adding additional faculty to expand our modeling expertise. In Phase 3 we have four Aims: (1) Support faculty to carry out model-based, interdisciplinary biomedical research and increase their competitiveness for external funding. Research in the Center is carried out in the context of Working Groups—zero-barrier, interdisciplinary, goal-focused teams that meet regularly to get work done. Supported research includes Pilot Projects, Modeling Access Grants, Data Access Grants and ad hoc teams. Our comprehensive plan for proposal preparation improves grantsmanship, and our staff assists with submission and grant management. (2) Increase University of Idaho’s faculty participation in biomedical research. We will invest time and resources in the existing faculty by providing mentoring, proposal development assistance, and social writing events. (3) Extend the reach of the Modeling Core into new areas of modeling to capitalize on emerging opportunities. The Modeling Core will develop Core Initiatives, focused on areas of modeling of broad interest to the campus community with high potential for growth. The first such initiative will be on digital twins. (4) Establish a path to long-term sustainability under the umbrella of the Institute for Modeling Collaboration & Innovation. A key strategy for sustainability is to maintain our status as a university institute; this provides funds for staff and Modeling Core postdocs. We will maintain engagement by Center participants to catalyze interactions and promote future interdisciplinary biomedical projects.

NIA - National Institute on Aging

The Center for SUNSHINE (Seniors Uniting Nationwide to Support Health, INtegrated care, and Economics) focuses on resilience, defined as the integrated capacity of individuals, families, healthcare systems, and communities to adapt to and support aging populations with complex health needs. SUNSHINE’s overarching mission is to advance aging resilience by integrating healthcare systems, public health organizations, social service agencies, and community-based resources to enhance the well-being of older adults and their care partners, and maximize societal value. SUNSHINE focuses on four key research areas: (1) healthcare systems, social services, and public health support; (2) social and behavioral factors of health across the life course; (3) cognitive and behavioral health; and (4) population-level interventions and resilience. These focus areas are supported by SUNSHINE’s three transformative aims: (1) facilitating interdisciplinary research to advance resilient aging, (2) training the next generation of resilience-focused researchers, and (3) translating research findings into real-world impact. SUNSHINE builds on a strong foundation, including the 50-year legacy of the University of Maryland Center on Aging and the advanced computational and learning health system infrastructures of the University of Maryland Institute for Health Computing. The interdisciplinary team unites expertise from ten units at the University of Maryland at College Park, including the newly established Artificial Intelligence Interdisciplinary Institute, and six units at the University of Maryland at Baltimore. SUNSHINE establishes a shared platform that bridges disciplines such as economics, demography, medicine, population health, AI/ML, epidemiology, and health informatics. A key strength of SUNSHINE lies in its proven success in collaborating with Historically Black Colleges and Universities to build research capacity. To effectively bridge research and policy, SUNSHINE leverages longstanding relationships and engages policymakers and community leaders through the Legacy Leadership Institute on Public Policy and AARP, ensuring its findings promote resilience for all aging populations. SUNSHINE is deeply committed to cultivating the next generation of researchers to advance resilience in aging and maximize societal value. SUNSHINE administers a pilot grant program that supports scholars in conducting high-impact resilience-focused aging research and supports scholars through tailored mentoring, multidisciplinary networking, and robust training programs. SUNSHINE is positioned to drive transformative research in resilience-focused aging, train the next generation of scholars, and bridge the gap between research and policy. These efforts will deliver innovative solutions that improve health and well-being for aging populations, addressing critical challenges at individual, community, and systemic levels.

Center For Sound Literacy Foundation

Center For Sound Literacy Foundation is an active grantmaking foundation based in Kentwood, MI. Focus: education. Contact the foundation directly for current funding opportunities.