Grants

MA Film Office

Tax credits and payroll incentives for film, TV, and commercial production in Massachusetts.

$5K – $100K

filmtourism

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MA Historical Commission Grants

MA Historical Commission

Grants for historic preservation planning, survey, and rehabilitation of historic properties.

$5K – $100K

historic_preservation

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MA Life Sciences Center Grants

MA Life Sciences Center

Grants for biotech, life sciences research, and technology commercialization.

$25K – $500K

technologylife_sciences

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MA Universal Pre-K (UPK) Grants

early childhoodpre-kschool readiness

Massachusetts Department of Early Education and Care

Early childhood education grants supporting pre-K programs, childcare quality improvement, and school readiness initiatives in MA.

$40K – $500K

2026-07-01

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MA Veterans Services Grants

MA Dept of Veterans Services

Grants for veteran housing, employment programs, and support services.

$5K – $50K

veterans

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MacArthur Foundation Climate Solutions

John D. & Catherine T. MacArthur Foundation

Supports the transition to a clean energy economy, reducing greenhouse gas emissions, and advancing climate justice in the U.S. and globally.

$200K – $5M

climateclean energyclimate justice+1

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MacArthur Foundation Criminal Justice

John D. & Catherine T. MacArthur Foundation

Reduces over-incarceration through the Safety and Justice Challenge. Supports jurisdictions in reducing jail populations and addressing racial disparities.

$200K – $3.5M

criminal justiceincarceration reductionracial equity

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MacArthur Foundation Nigeria Programs

John D. & Catherine T. MacArthur Foundation

Supports governance, reproductive health, conservation, and accountability in Nigeria.

$50K – $1M

governanceHealthconservation+1

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Machine Learning as a Tool to Predict Early and Chronic Graft Dysfunction after Lung Transplantation

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Lung transplantation is the treatment of last resort for a large number of patients with end-stage lung diseases, but is complicated by a modest post-transplant survival. Mortality after transplantation is mostly driven by chronic lung allograft dysfunction (CLAD). An early complication of lung transplantation, primary graft dysfunction (PGD), is a major risk factor for subsequent development of CLAD. Tools to more accurately predict these complications are urgently needed. This proposal hypothesizes that integrating clinical and biological markers from donors and recipients will predict the incidence and severity of PGD and CLAD. This award will support the career development of a mathematician–data scientist toward a critical and underexplored area. The candidate has a strong foundation in mathematical modeling, machine learning, and biomedical data science, and aims to apply these skills to improve outcomes after lung transplantation. Through this K25 award, he will transition to an independent research career centered on translational, data-driven solutions to clinical challenges in transplant medicine. This will be achieved under the following Aims: Aim 1: Identify and validate predictors of PGD incidence and severity. Aim 2: Identify and validate predictors of CLAD onset and subtype. In pursuit of both Aims, we will obtain biospecimens from 3 anatomical sites (donor lung pre-transplant, donor lung 2 hrs post-transplant, and serially blood samples from the recipient) and donor and recipient clinical data from ≥200 patients at two large lung transplant centers. We will perform a multiplex assay measuring 71 cytokine/growth factors to screen samples for markers of cell activation, chemotaxis, injury, angiogenesis and growth factors. We will use computational phenotyping and machine learning to predict outcomes from these comprehensive biological and clinical data. These models will also allow us to identify novel markers for both outcomes that could improve mechanistic understanding and support point-of-care test design. Trained models and candidate markers will be validated using multiplex and ELISA assays of prospectively collected samples from recipients at two major transplant centers over the course of the study. The ability to predict PGD and to forecast CLAD onset are essential for the development of life-, health-, and graft-extending interventions. Our proposed project builds upon important ongoing work while introducing five advances: multi-site specimens, a broad-scope injury/immune response cytokine panel, analysis of conventional storage solution, specialized computational modeling, and multi-center validation. Successful completion of this project will yield externally validated biomarker panels for PGD incidence and severity and CLAD onset and subtype suitable for developing point-of-care tests.

Up to $143K

2031-03-31

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Machine Learning to Disentangle Neurobiological Heterogeneity in the Schizophrenia Spectrum Disease Course

NIMH - National Institute of Mental Health

PROJECT SUMMARY Schizophrenia is a neuropsychiatric disorder which lacks clinically actionable biomarkers to guide diagnosis, treatment, and prognostication. There are, however, well-replicated neurobiological findings in schizophrenia – namely, decreased hippocampal volume, widespread cortical thinning, and ventricular enlargement. Decades of work from our lab and others have established the hippocampus as central to the pathophysiology of schizo- phrenia, with structural and functional deficits associated with illness severity and cognitive dysfunction. Despite this, the clinical utility of hippocampal imaging remains limited, largely due to unresolved questions about the origin, trajectory, and heterogeneity of hippocampal pathology. Recent advances in machine learning have enabled innovative approaches to address these core questions and disentangle the known individual- level heterogeneity in schizophrenia, revealing potential disease subtypes with distinct progression patterns. This work both identifies several possible epicenters of disease (including the hippocampus) and suggests a network-based progression model via which pathology spreads along the brain’s white matter tracts (i.e., the connectome). Notably, our work suggests an important structural and functional differentiation between the anterior and posterior hippocampus, implicating the former as crucial during the early stages of psychosis. Given this context, I hypothesize that schizophrenia is not a unitary disease, but comprises multiple subtypes with distinct spatiotemporal patterns of gray matter degeneration, including a subtype in which pathology originates in the anterior hippocampus and propagates through its structural connectome. To test this hypo- thesis, we will integrate advanced machine learning with longitudinal modeling using MR imaging, uniquely leveraging our lab’s rich data and technical expertise. In Aim 1, I will characterize group-level patterns of gray matter volume (GMV) change over the first decade of psychotic illness, stratified by clinical trajectory, using longitudinal structural modeling. In Aim 2, I will apply a cutting-edge machine learning algorithm – Subtype and Stage Inference (SuStaIn) – to a large, cross-sectional discovery sample to identify latent disease subtypes based on inferred patterns of GMV progression. In Aim 3, I will evaluate the external validity of these subtypes using our in-house longitudinal cohort of psychosis patients (see Aim 1). This will be the first study to utilize SuStaIn to specifically probe the differential roles of the anterior and posterior hippocampus in the patho- physiology of psychosis and will directly test the hypothesis that disease emerges and propagates along structural brain networks. By integrating machine learning with longitudinal neuroimaging, these experiments will identify and validate biologically grounded subtypes of schizophrenia, probing key features of hippocampal pathology and offering insight into hippocampal dynamics across illness stages. This innovative approach addresses a longstanding barrier in schizophrenia research – its vast clinical and neurobiological heterogeneity – and has potential to transform diagnosis, monitoring, and treatment following a first episode of psychosis.

Up to $36K

2030-05-31

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Maclellan Foundation Christian Ministry Grants

Maclellan Foundation

Supports strategic global Christian ministries focused on the unreached. Funds evangelism, discipleship, Bible translation, and leadership development.

$25K – $250K

evangelismdiscipleshipBible translation+1

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Macroinvertebrate assemblages along the Tuolumne River below Hetch Hetchy Reservoir

National Park Service

United State Department of the Interior, National Park Service (NPS) Notice of Intent to Award. This is not a request for applications. This funding opportunity is to provide public notice of NPS's intention to fund the following project activities without full and open competition. Task Agreement #P16AC01801 under Cooperative Agreement P13AC000676 with the University of California, Los Angeles, a partner under the Californian Cooperative Ecosystem Studies Unit, for project titled "Macroinvertebrate assemblages along the Tuolumne River below Hetch Hetchy Reservoir"

Up to $65K

natural resources

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Macrophage Derived Small Extracellular Vesicles to Resolve Spinal Cord Injury Induced Pain

NINDS - National Institute of Neurological Disorders and Stroke

Project Abstract Neuropathic pain is a common complication of spinal cord injury (SCI), characterized by symptoms of allodynia and hyperalgesia experienced at- and below the level of injury. This type of chronic pain can be spontaneous or evoked, and currently accepted therapeutics display limited efficacy. Neuroimmune interactions are thought to play a central role in the development and maintenance of neuropathic pain. Increased production of proinflammatory mediators after SCI alters the expression of voltage-gated channels on primary nociceptors, driving hypersensitivity and spontaneous activity. This results in aberrant sensory signaling extending from the peripheral dorsal root ganglia (DRG) into the spinal dorsal horn and ascending to supraspinal centers, driving neuropathic pain. Intercellular communications between infiltrating macrophages and neuronal populations in the DRG after injury have drawn considerable interest in the study of neuropathic pain, as these cells have critical contributions to both the development and resolution of chronic pain. Recent work highlights the therapeutic potential of small extracellular vesicles (sEVs) derived from lipopolysaccharide (LPS)-stimulated macrophages in preclinical models of inflammation and pain. Preliminary data from our lab revealed a dramatic resolution of established SCI-induced neuropathic pain and a more normal distribution of nociceptive primary afferents in the spinal cord after intrathecal injection of sEVs released from RAW 264.7 macrophages treated with LPS. However, how sEVs affect nociceptors and/or other cells found along the sensory neuroaxis remains to be established. We hypothesize that sEVs from LPS-stimulated macrophages attenuate aberrant nociceptor plasticity and hyperexcitability to resolve neuropathic pain after SCI via 1: direct internalization by nociceptors in the DRG, or 2: indirectly by affecting endogenous macrophage/microglia mediated mechanisms. Two specific aims have been developed to explore this hypothesis. Our first aim will utilize patch clamp electrophysiology recordings to determine how DRG nociceptors are affected by sEV administration both in vitro and in vivo. The second aim will deplete endogenous macrophages and microglia in hypersensitive SCI rats to determine whether these cells are necessary for the analgesic effect of sEV administration. The data from this proposal will explore how macrophage derived sEVs interact with the neuroimmune environment after SCI in a way that facilitates treatment of neuropathic pain.

Up to $50K

2028-05-31

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Macrophage handling of particulate-laden cell corpses disrupts immunometabolism

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY Bioaccumulation of particulate matter (PM) in the lungs is a key feature driving pulmonary disease development in the modern world, with 4.2 million deaths per year reported by the World Health Organization from ambient air exposure alone. Alveolar macrophages (AM) are professional phagocytes that comprise 95% of the leukocyte population in the alveoli, critical to maintaining systemic health and protection from environmental exposures by clearing pathogens, foreign particulates, and cell corpses from the alveolar space. However, the fate of non- degradable PM contained within macrophages (MΦ) following cell death is unknown. Previous work from our group shows that cell corpses transfer their endogenous metabolites to AM upon clearance, triggering anti- inflammatory metabolic and immune reprogramming in the engulfing AM. We hypothesize that any non- degradable PM contained within a cell corpse will also be transferred to the engulfing MΦ, and that the presence of PM will perturb MΦ immunometabolic reprogramming to instead promote chronic inflammation. We further hypothesize that the level of perturbation will differ between apoptotic versus necrotic cell death, with elevated disruption following engulfment of PM-exposed necrotic cells (NC). Using in vitro and in vivo systems, we will first expand upon our preliminary experiments investigating the characteristics of PM transfer from cell corpses to live MΦ, examining PM2.5 and amorphous silica. Preliminary studies indicate that the type of cell death impacts the way PM is transferred. Using a cytoskeletal inhibitor screen, we identified two compounds effective at blocking corpse uptake, but not PM transfer from NC to live MΦ. These findings provide tools we can use to study this unique mode of transfer. We also found that PM transfer from cell corpses impacts MΦ transcriptional reprogramming in response to corpse engulfment. Preliminary examination of MΦ response to PM10-exposed apoptotic cells (AC) or NC identified an upregulation of proinflammatory and metal response genes in engulfing MΦ when engulfed corpses contained PM10. Examining PM2.5, we will extend these preliminary studies of MΦ reprogramming to investigate the impacts of PM2.5-laden corpse engulfment on MΦ cytokine production and metabolism. Finally, a novel bone marrow chimera model will be used to study the endogenous in vivo response of recruited AM engulfing PM2.5-laden versus naïve apoptotic resident AM corpses. The transcriptome and metabolome of recruited AM sorted by engulfment will be assessed to characterize how the presence of PM in cellular corpses alters AM immunometabolic programming following engulfment in vivo. This proposal will address gaps in knowledge regarding AM and inhaled particulates that will advance our understanding of how PM exposures promote the development of chronic lung inflammation and disease.

Up to $35K

2029-04-19

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Macrophage one-carbon metabolism in atherosclerotic plaque stability

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY/ABSTRACT Atherosclerotic cardiovascular disease (ASCVD), driven by the buildup of fibrofatty plaques in arterial walls, remains the leading cause of death worldwide. Plaque instability, characterized by foam cell apoptosis and impaired efferocytosis, the process by which macrophages clear apoptotic cells, leads to rupture and life- threatening cardiovascular events. In contrast, enhancing efferocytosis by macrophages can promote plaque stability and atherosclerosis regression. Despite significant advances in lipid-lowering therapies, residual ASCVD risk persists, highlighting an urgent need for novel therapeutic targets to stabilize rupture-prone plaques and promote atherosclerosis regression. Recently, we and others identified a critical role for dysregulated amino acid metabolism in ASCVD, consistently demonstrating reduced circulating glycine. Glycine is primarily synthesized from serine by serine hydroxymethyltransferase 2 (SHMT2), which initiates the one-carbon metabolism (1CM) pathway. While 1CM has been extensively studied in cancer, its role in ASCVD is poorly understood, and the impact of macrophage 1CM in atherosclerosis is unknown. Here, we found that macrophage SHMT2 is suppressed as atherosclerosis advances in humans and mice. Using our novel myeloid-specific SHMT2-deficient (Shmt2MKO) mice, we discovered that SHMT2-dependent 1CM in macrophages is crucial for maintaining plaque stability features. Stable-isotope tracing uncovered that SHMT2 loss in macrophages disrupts 1CM leading to inhibition of de novo glutathione synthesis, redox imbalance, and overproduction of serine-derived ceramides. Transcriptomics revealed a suppression of key cytoskeleton remodeling and phagosome regulators, aligned with defective efferocytosis that was rescued by restoring SHMT2. This proposal will address the central hypothesis that impaired SHMT2-dependent 1CM in macrophages drives plaque instability by disrupting efferocytosis through altered redox and ceramide metabolism, while restoring SHMT2 enhances features of plaque stability and atherosclerosis regression. Aim 1 will define the mechanisms by which SHMT2-dependent 1CM drives efferocytosis, elucidate the mechanisms by which macrophage SHMT2 is suppressed by proatherogenic stimuli, and characterize impaired 1CM in human and mouse lesional macrophages using our Shmt2MKO mice, newly generated mice lacking rate-limiting enzymes of glutathione and ceramide synthesis, as well as pharmacological, metabolomics, and novel mass spectrometry imaging approaches. Aim 2 will establish impaired SHMT2- dependent 1CM in macrophages as a driver of plaque instability in atherosclerosis progression and regression, determine redox imbalance, ceramide overproduction, and defective efferocytosis as underlying mechanisms, and evaluate the therapeutic potential of restoring SHMT2 in lesional macrophages using our new mouse models in the Ldlr-/- background, and our validated macrophage-targeting nanoparticle platform. Successful completion of this proposal will define a novel metabolic pathway linking efferocytosis and plaque stability and identify a new target to stabilize rupture-prone atheromas and promote atherosclerosis regression, critical unmet clinical needs.

Up to $737K

2030-01-31

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Macrophages in human autoimmune tissue pathology

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY Rheumatoid arthritis (RA) compromises the health of ~1% of the population, and identifying a medication that works well for a given individual is challenging. It remains unclear why RA patients respond differently to the same medications, and some remain refractory to all treatments. It is believed that RA may encompass several endotypes driven by distinct pathogenic mechanisms that would be responsive to distinct therapies. To this end, large-scale studies have recently identified putative endotypes defined by synovial tissues molecular patterns. This includes efforts in the UK (led by Pitzalis) and in the U.S. (by the Accelerating Medicines Partnership (AMP) consortium), where both studies concluded that up to one-third of RA patients have myeloid-rich synovial tissue, notably distinct from the widely described lymphocyte-rich tissues. Data from the AMP report (Zhang et al. Nature 2023), identified that the predominant myeloid population in myeloid-rich tissues is a non-inflammatory monocyte-derived macrophage state. Our preliminary data cross referencing transcriptomic datasets show that the signature of “non-inflammatory” macrophages in RA joints resembles that of Pro-Fibrotic monocyte-derived macrophages from tissues affected by fibrosis. Further, we have defined their functional pathways to include wound-healing/fibrosis, coagulation, lipid metabolism, and proliferation (markers including: SPP1, SERPINE1, FABP5, and CSF1, respectively). Using spatial transcriptomics, we now find these RA synovial Pro-Fibrotic macrophages at high densities in fibrin-rich deposits at the synovial lining. In healing wounds, fibrin deposits serve as a template for the generation of new connective tissue. Notably, the synovium lacks an epithelial layer that, in other tissues, limits where the new tissue can form. Thus, we hypothesize in RA synovium, Pro-Fibrotic macrophages together with fibroblasts and fibrin matrices drive pathologic tissue outgrowth and that targeting this process will reduce pannus formation. We therefore aim to define how Pro-Fibrotic macrophages differentiate in RA synovium and modify fibrin deposits using paired single-nuclei transcriptomics-epigenomics analyses and assays testing fibrin coagulation, degradation and ingestion (Aim 1). To determine how Pro-Fibrotic macrophages impact RA synovial tissue outgrowth, we will use spatial transcriptomics of RA patient synovium to quantify the extent of Pro-Fibrotic macrophage localization to fibrin deposits, and test how Pro-Fibrotic macrophages embedded in fibrin impact synovial fibroblast entry and collagen production using a microfluidic chamber system (Aim 2). Lastly, we will test how “anti-inflammatory” RA medications (e.g. methotrexate, TNFi, IL6Ri) affect Pro- Fibrotic and Inflammatory macrophages in RA patient synovial ex vivo drug assays and in fibrin coagulation and clearance assays. Using data from the new AMP-AIM consortium, we will test how patient drug response rates relate to Pro-Fibrotic macrophage (v. lymphocyte) levels in synovial biopsies via spatial transcriptomics (Aim 3). Completion of these aims will extend our understanding of mechanisms underlying treatment discrepancies and advance development of precision treatment strategies in RA patients based on molecular patterns of disease.

Up to $569K

2031-05-31

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Macrosystems Biology

U.S. National Science Foundation

The Macrosystems Biology: Research on Biological Systems at Regional to Continental Scales will support quantitative, interdisciplinary, systems-oriented research on biosphere processes and their complex interactions with climate, land use, and invasive species at regional to continental scales as well as planning and development activities to enable groups to conduct Macrosystems Biology Research.

$250K – $5M

sciencetechnology

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Macrosystems Biology and NEON-Enabled Science

U.S. National Science Foundation

TheMacrosystems Biology and NEON-Enabled Science (MSB-NES): Research on Biological Systems at Regional to Continental Scalesprogram will support quantitative, interdisciplinary, systems-oriented research on biosphere processes and their complex interactions with climate, land use, and changes in species distributionatregional to continental scales as well as training activities to broaden participation of researchers in Macrosystems Biology and NEON-EnabledScience. MSB-NES projects that use data and/or resources fromthe National Ecological Observatory Network(NEON) are encouraged. Substantive NEON-enabled projects rely on data and/or samples collected by NEON and/or co-locate research activities at NEON sites. Projects may develop tools that will explicitly enhance the processing, use, and/or analysis of NEON data or collections, in the context of addressing a specific research question or hypothesis. However, proposals primarily focused on tool development that can be used for a broad class of research questions or for topics that meet the needs of a community of researchers should be directed toward the Infrastructure Innovation for Biological Research (Innovation) or Infrastructure Capacity for Biological Research (Capacity) programs in the Division of Biological Infrastructure.

sciencetechnology

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Madison Community Foundation Community Grants

Madison Community Foundation

Madison Community Foundation ($350M in assets) supports nonprofits in WI through grants focused on education, community development, health, arts. Awards range from $2,000 to $100,000.

$2K – $100K

Educationcommunity developmentHealth+1

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Madrona PK-8 Playground Revitalization Design

Madrona PTSA

Madrona PK-8, a Title I school in central Seattle, will replace its aging playground with an engaging play structure that will allow the grounds to be open to the public outside of school hours. The redesign will improve transitions, redo the landscaping, and accommodate the growing school. This grant will pay for design and construction documents.

Up to $25K

Educationinfrastructure

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Magnetic resonance imaging methods to capture tolerogenic cell therapy fate in preclinical and ex vivo human transplant models

NIBIB - National Institute of Biomedical Imaging and Bioengineering

ABSTRACT Solid organ transplantation has transformed care for patients with end-stage organ failure, dramatically improving survival and quality of life. In 2024, over 48,000 transplants were performed in the United States. Despite advances in immunosuppressive regimens, allograft rejection remains a major barrier to long-term graft survival, with 25–50% of recipients experiencing rejection. While effective at reducing early rejection, current immunosuppressive therapies carry significant long-term toxicities and have not meaningfully extended graft survival. This has driven the search for safer alternatives to promote immune tolerance. Adoptive transfer of regulatory T cells (Tregs) offers a promising immunomodulatory strategy to promote graft tolerance while minimizing systemic toxicity. However, without tools to monitor Treg trafficking and functionality, it is challenging to assess treatment efficacy or optimize therapeutic strategies. Magnetic resonance imaging (MRI) is ideally suited for this purpose—it is widely available, radiation-free, and capable of high-resolution imaging of labeled cells. Conventional MRI-based cell tracking relies on exogenous contrast agents such as iron oxide or fluorine compounds, which require labor-intensive labeling protocols often involving non-FDA-approved transfection agents that may impair cell viability or function. These challenges limit clinical scalability and regulatory approval. We propose a fundamentally different approach: the magnetic microbeads used in the process of Treg purification from blood leukapheresis will directly label the target cells, producing proton (1H) MRI contrast. Our goal is to develop magnetic resonance imaging methods to capture tolerogenic cell therapy fate in preclinical and ex vivo human transplant models. We propose the following aims: AIM 1 will capture longitudinal Treg activity in a murine transplant model. We will isolate and label mouse Tregs with CD25/CD4 beads, evaluate phenotype and cytokine expression, and infuse them into matched and mismatched skin and heart graft models to confirm preferential homing of injected Tregs in matched skin transplants via MRI followed by histopathology correlation. AIM 2 will evaluate immunomodulatory cell trafficking and imaging feasibility in a clinically relevant ex vivo human organ model. We will infuse microbead-labeled Tregs into discarded donor organs maintained on normothermic perfusion pumps. This platform will enable us to investigate critical questions about Treg and other immunomodulatory cell behavior post-infusion, including their distribution patterns, retention over time, and interaction with vascular and tissue compartments. This work will enable real-time monitoring of therapeutic cell fate, improve patient-specific immunosuppression strategies, and accelerate safe translation of Treg-based therapies for transplantation, autoimmunity, and beyond.

Up to $547K

2030-03-31

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Magnetic resonance true temperature imaging with high spatial and temporal resolution

NIBIB - National Institute of Biomedical Imaging and Bioengineering

ABSTRACT The knowledge of temperature and temperature distribution within the brain can be critical to understanding the healthy and diseased brain, its response to acute injury, and in monitoring critically important thermal interventions. There are several temperature sensitive properties such relaxation rates and the proton resonance frequency shift (PRFS) that can be measured with magnetic resonance imaging (MRI) methods but these methods can only measure temperature change. The PRFS method, which provides the most accurate measurement of temperature change can only measure true tissue temperature if the starting true temperature distribution is known. Fortunately, MR spectroscopy (MRS) methods have been developed that show great promise in the measurement of true temperature. These methods rely on the detection of a temperature independent spectral peak of protons bound to carbon atoms in high concentration metabolites, such as N- acetylaspartate (NAA), creatine (Cr) and choline (Cho) which can be used as a reference for the temperature dependent spectral peak of water protons. Both single voxel spectroscopy (SVS) methods and MRS imaging (MRSI) methods have been described but are slow because of the long readout time needed to achieve adequate spectral resolution and the need to perform multiple averages due to the low signal being measured. Echo-planar spectroscopic imaging (EPSI) speeds up MRSI by interleaving an oscillating imaging gradient to spatially encode one of the imaging dimensions simultaneously with spectral readout. Unfortunately, SVS, MRSI, and even EPSI are unsuitable for clinical applications because of the low spatial resolution (voxel size 1 cm3) and temporal resolution (multiple minutes). The goal of this project is to develop an MRI technique that can measure true temperature in the whole brain at spatial and temporal resolutions that enable clinical utility for acutely assessing and longitudinally monitoring healthy and diseased brain tissue, and real time monitoring of thermal interventional therapies. This innovative true temperature measurement technique combines EPSI, for low resolution background field measurements, with PRFS for high spatial and temporal resolution water proton measurements. While conventional EPSI methods interleave volumetric acquisitions with and without water suppression, we propose an innovative modification to take advantage of the very strong water signal to obtain a very high resolution, dynamic method for true temperature measurements. The MRI pulse sequence will be refined, validated (Aim 1), applied to healthy subjects and post-surgery patients at risk for infections (Aim 2), and applied to essential tremor (ET) patients during the required delay between repeated focused ultrasound sonications (Aim 3). Successful completion of the aims of this study will result in a clinically practical method to obtain true temperature measurements in the brain with a spatial and temporal resolution sufficiently high to meet the needs of monitoring focal thermal therapy treatments as well as to provide true temperature measurements over the entire brain for assessment of the state of the brain with disease, infection, and injury.

Up to $231K

2028-05-31

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Magnetospheric Physics

U.S. National Science Foundation

Supports research on the magnetized plasma envelope of the outer atmosphere, including energization by the solar wind; the origin of geomagnetic storms and substorms; the population by solar and ionospheric sources; the origin of electric fields; the coupling among the magnetosphere, ionosphere, and atmosphere; and waves and instabilities in the natural plasma. Also supported are ground-based observational programs at high latitudes and laboratory experiments applicable to the geospace environment. Theoretical research programs may include numerical simulations using a variety of MHD, hybrid and particle codes. The analysis of data from all sources, whether ground-based or from spacecraft, is also supported.

sciencetechnology

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Magnolia Beautification IV/V - 2023

Magnolia Chamber of Commerce

The goals of Phases IV and V are to create a Parklet on 33rd Ave W in the heart of the business district (with tables, chairs, benches and bike racks), and install benches/bike racks on 33rd and 32nd W. There are no parks with seating areas near Magnolia's downtown. In 2017/2018, volunteers installed `one-day demonstration Parklets` that were met with great enthusiasm by community members and businesses, who support creating a permanent Parklet. (Photos included). Phases IV/V will strengthen and expand community partnerships we have developed, with Magnolia businesses, City Departments such as SDOT, community volunteers and our broad base of donors.

Up to $41K