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Maine Community Foundation

Maine Community Foundation ($800M in assets) supports nonprofits in ME through grants focused on education, arts, environment, community development. Awards range from $1,000 to $100,000.

Manitoba Arts Council

MAC provides grants to artists and arts organizations in Manitoba for creation, production, presentation, and community engagement across all art forms.

Maple Leaf Community Council

The Maple Leaf Summer Social 2023 is a free and public party in Maple Leaf Reservoir Park featuring food (including LOTS of free ice cream), games, music, art, and most importantly, the opportunity for participants to make vital post-pandemic connections with old and new neighbors.

Maryland Council on the Arts

General operating support grants for arts organizations in Maryland. Funded by the National Endowment for the Arts and state appropriations.

Maryland Council on the Arts

Project-based grants for arts programming, performances, exhibitions, and community engagement in Maryland.

Maryland State Arts Council

Maryland State Arts Council provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across MD.

Massachusetts Cultural Council

Massachusetts Cultural Council provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across MA.

Massachusetts Cultural Council

The Cultural Investment Portfolio (CIP) provides general operating support grants to established Massachusetts cultural organizations, enabling them to deliver arts, humanities, and interpretive science programs of public benefit.

Massachusetts Cultural Council

The Local Cultural Council (LCC) Program distributes grants through 329 local cultural councils to support arts, humanities, and interpretive science programs that engage the public across Massachusetts communities.

McKnight Foundation

The McKnight Foundation funds nonprofits, artists, and researchers in Minnesota and beyond in areas including arts and culture, Midwest climate and energy, Mississippi River, neuroscience, international programs, and regional grantmaking.

ME Arts Council

General operating and project support for arts organizations and individual artists in ME. Funds visual arts, performing arts, literary arts, and arts education.

NIEHS - National Institute of Environmental Health Sciences

ABSTRACT The Measuring Micro- and Nanoplastics in Environmental Samples Workshop (“the Workshop”) will be held as part of a Great Lakes Microplastic and Health Symposium (June 17-18, 2026) in Rochester, New York. This Workshop aims to pool existing expertise, establish new collaborations, and prioritize future needs for characterizing micro- and nanoplastics (MNP) in complex environmental matrices relevant to health research in the Great Lakes ecosystem. This Workshop will bring together national experts on MNP analysis with researchers studying the interactions between Great Lakes ecosystems (particularly water and air) and health. The Workshop will be hosted by two multidisciplinary centers that are part of the NIH/NSF Centers for Oceans and Human Health program. The University of Rochester and Rochester Institute of Technology co-host the Lake Ontario MicroPlastics (LOMP) Center, a transdisciplinary hub for research, translation and engagement on how MNPs affect human health and the Great Lakes environment (particularly water and near shore air). The Great Lakes Center for Fresh Water and Human Health is based at the University of Michigan (the Great Lakes Center). Its central goal is to better understand the increasing risks that cyanobacterial harmful algal blooms (cHAB) pose to freshwater ecosystems and human health. One aspect of the Great Lakes Center’s research is to explore the association of aerosolized microplastics and cHABs. Fostering collaboration and scientific exchange between the Great Lakes Center, LOMP, and national experts studying MNPs is one example of how this workshop may have long-term impacts on regional MNP research collaborations that may yield results of global significance. The Workshop has three objectives: 1) Bring together scientists from multiple laboratories and institutions to present new findings, identify methodological challenges, and share analytical approaches to better understand environmental exposures to MNPs and their potential impact on human and environmental health; 2) Develop new collaborations between researchers and trainees across institutions, both regionally and nationally; and 3) Identify priorities and opportunities for analytical advances to support this rapidly growing field. The objectives will be met through a Workshop format with a limited number of participants (30-40) to encourage close interaction. The requested R13 conference funds will be used to pay for expenses for the June 17 Workshop, including travel expenses for trainees, invited experts, and researchers from other institutions. R-13 support will also enable these attendees to participate in the full Great Lakes Microplastic and Health Symposium, to be held on June 18 at the University of Rochester’s Memorial Art Gallery, that will include a larger number of researchers, trainees, and community partners (120-150) on a broad range of topics related to Microplastics and Health with a focus on the Great Lakes region.

NIGMS - National Institute of General Medical Sciences

Predictions of drug disposition and toxicity from preclinical data, estimation of risk of drug-drug interactions and simulation of drug exposures in humans are essential for safe and effective drug development and clinical pharmacology. Despite decades of research, significant gaps still remain in translating preclinical findings to clinical drug development and practice. As a result, about 90% of drug candidates that enter Phase I clinical trials fail during development. In addition, uncertainty regarding the disposition characteristics of approved drugs often remains after drug approval leading to post marketing studies and label revisions. This wastes resources, leads to unnecessary risk to patients and limits access to life saving medications for specific patient populations. My laboratory works to bridge the knowledge gaps in translational science via mechanistic in vitro studies, mass spectrometry based proteomics experiments and state-of-the art in silico modeling. We develop novel proteomics methods to understand formation of drug adducts by small molecule drugs, evaluate how drug-protein and protein-protein interactions within a cell alter drug distribution and the activity of drug metabolizing enzymes, and assess how genetic variability and individual biology such as sex, disease and age alter drug exposures in tissues and in blood. Central questions of my research program include: What mechanisms cause significant under and overpredictions of drug exposures and drug-drug interactions in humans? Which individual factors define interindividual variability in drug-protein adduct formation making certain individuals highly susceptible? What mechanisms lead to changes in drug clearance in specific populations and between individuals? Answering these questions will advance developing individualized therapy and enable connecting observable patient specific factors with decisions of drug dosage adjustments. Our long term goal is to improve the preclinical, translational and computational methodologies used to predict and evaluate drug disposition and adverse drug reactions. Our current studies are focused on 1) development of innovative proteomic methods for discovery, characterization and quantification of protein adducts in simple and complex biological matrices; 2) evaluation of the role of fatty acid binding proteins in modulating tissue drug distribution and drug clearance and 3) developing novel physiologically based pharmacokinetic models to predict drug disposition in specific populations including vulnerable patients. Our studies advance innovative areas such as how intracellular binding proteins influence drug efficacy, and provide unprecedented insight into mechanisms of enzyme inactivation and quantitative relationships between adduct formation and metabolic activity in the liver. Our research will also provide open and accessible cutting-edge tools for high-dimensional proteomics data and novel PBPK models for prediction of drug disposition in specific patient populations. Our work promises to decrease failure rate during drug development and lead to expanded access to approved medications in specific patient groups through improved quantitative systems biology approaches.

National Institutes of Health

-Purpose. This Funding Opportunity Announcement (FOA) issued by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), the National Cancer Institute (NCI), and the Office of Dietary Supplements (ODS), National Institutes of Health (NIH), solicits grant applications from institutions/organizations that propose to employ an integrative approach using state-of-the-art technologies to gain insight into the molecular and biochemical mechanisms by which chronic alcohol consumption leads to the development of cancers of various organs such as oral cavity, pharynx, larynx, esophagus, stomach, large intestine, liver, and breast. This includes investigating roles of various factors such as acetaldehyde, cytochrome P450 2E1 (CYP2E1), vascular endothelial growth factor (VEGF), impaired immune function, and alcohol-induced impaired metabolism of s-adenosylmethionine (SAMe), folate, betaine, iron, and vitamin A. -Mechanism of Support. This FOA will utilize the NIH Research Project Grant (R01) award mechanism and runs in parallel with an FOA of identical scientific scope, PA-06-270, that solicits applications under the Exploratory/Developmental (R21) grant mechanism.

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary Due to the progressive depletion of CD4+ T cells, HIV/AIDS patients are more susceptible to infection of Cryptococcus neoformans, an encapsulated fungus that is listed by WHO as a pathogen of critical priority. An estimated 112,000 people die from C. neoformans infections globally each year. C. neoformans is a leading cause of mortality among HIV/AIDS patients. Antiretroviral therapy (ART) can rapidly restore CD4+ T cells in HIV/AIDS patients, representing a major advance in the treatment of HIV-infections. However, the rapid recovery of CD4+ T cells in HIV/AIDS patients that co-infected with C. neoformans after initiation of ART often causes an exaggerated inflammatory response in the central nervous system (CNS), termed immune reconstitution inflammatory syndrome (IRIS). Cryptococcal IRIS is considered as a life-threating condition, as it can lead to a high mortality rate during ART among HIV/AIDS-associated IRIS patients who have a cryptococcal infection. Clinical studies have shown that cryptococcal IRIS is associated with a substantial CNS recruitment of immune cells and enhanced secretions of inflammatory cytokines. However, the cellular and molecular mechanisms involved in cryptococcal IRIS are poorly understood. In particular, it remains to be determined which leukocyte subset(s) and cytokine(s) mediate the death during cryptococcal IRIS and how CD4+ T cell responses are regulated during cryptococcal IRIS. These questions are hard to be answered without animal studies. Using a novel murine model of C. neoformans infection to closely mimic HIV/AIDS-associated cryptococcal IRIS, we will define the mechanisms of cryptococcal IRIS by addressing the following aims: 1) To identify the leukocyte subset(s) accounting for lethal cryptococcal IRIS; 2) To identify the cytokine(s) accounting for lethal cryptococcal IRIS; 3) To identify the factors regulating CD4+ T cells responses during cryptococcal IRIS. Successful completion of this study would gain novel insights into the cellular and molecular mechanisms that mediate lethal immune responses during cryptococcal IRIS and identify potential targets for treatment of HIV/AIDS-associated cryptococcal IRIS patients.

NIGMS - National Institute of General Medical Sciences

PROJECT SUMMARY/ABSTRACT Dynamic interactions between intercellular membranes and the cortical cytoskeleton are critical for cell survival. During their normal functions, cells face physiological and environmental stresses that can lead to rupture of the plasma membrane and/or of the nuclear envelope. Rapid repair of such injuries, whether arising from daily activities or resulting from trauma, infection, or diseases such as cancer, is an active area of cell biology research. My lab has a long-standing track record in successfully identifying key molecules and elucidating their in vivo roles at the cell cortex necessary for the repair of plasma membrane and at the nuclear envelope necessary for repair of the nuclear cortex. The overall focus of the lab is to delineate how cells deal with such cell and/or nuclear cortex disruptions to efficiently and effectively repair the lesions. We have developed a robust inducible single cell repair model using the syncytial Drosophila embryo that has superb amenability for live imaging and genetic tractability that is unavailable in other cell wound repair models. We have also established a model for the newly appreciated nuclear export pathway (Nuclear Envelope budding) on the surface of Drosophila salivary gland and S2 cell nuclei that provides the same superb amenability for live imaging and genetic approaches. While both systems rely heavily on dynamic membrane and/or cytoskeleton/nucleoskeleton interactions, a major challenge in both of these systems is the absence of a molecular outline of the events occurring during the repair and/or export processes in any organism or system. Our goals during the proposed period are to establish the molecular framework underpinning these processes using a combination of state-of-the-art cell biological, genetic, developmental, biochemical, and high-resolution imaging approaches. Our studies are expected to be of significant medical relevance, as understanding the molecules, machineries, and pathways governing cell wound repair, NE-budding (nuclear export), and dynamic membrane-cytoskeleton/nucleoskeleton interactions will be extremely valuable for elucidating fundamental cellular mechanisms, as well as for developing new or enhancing existing strategies for treating conditions associated with cell/nuclear damage, and for disciplines such as regenerative medicine where cell based constructs are used to reconstruct tissues, clinical drug delivery systems where molecules cross cell membranes, and for virus nuclear egress.

NIEHS - National Institute of Environmental Health Sciences

PROJECT SUMMARY Micro-nano-plastics (MNPs) are small plastic particles resulting from the environmental breakdown of plastic waste over time. These particles have accumulated in ecosystems and entered the food web through contaminated water and food, trophic transfer, and exposure during food processing and packaging. Recent studies have detected MNPs in nearly every human organ and tissue, underscoring their widespread presence. While it is known that MNPs can cross biological barriers like the intestine, the health effects of MNP exposure are still poorly understood, and the mechanisms that allow MNPs to bypass these barriers remain unclear. Additionally, most toxicological studies have relied on simplified MNP models, such as polystyrene beads, which do not accurately reflect the complex physicochemical properties of real-world MNPs. This project aims to bridge these knowledge gaps by exploring the intestinal uptake mechanisms, biodistribution, and impacts on intestinal health of environmentally relevant MNPs. The focus will be on the effects of MNP polymer type, size, surface chemistry (including weathering), and prolonged exposure on MNP toxicity and inflammatory responses. Our central hypotheses are: (I) MNP properties such as size, polymer type, and environmental weathering influence their uptake, translocation, toxicity, and inflammatory effects; (II) MNPs are taken up through both passive diffusion and energy-dependent endocytosis pathways; (III) prolonged exposure enhances MNP uptake by altering gene expression related to cell junctions, endocytosis, and inflammation; and (IV) intestinal inflammation, such as in inflammatory bowel disease (IBD), increases MNP translocation by enhancing intestinal permeability, which further promotes biodistribution. To achieve these objectives, the study is organized into two specific aims: Aim 1: Synthesize and characterize environmentally relevant “tracer” MNPs (Au Core-Plastic Shell) for use in toxicological studies. These physicochemically characterized MNPs will be subjected to weathering/aging processes to simulate environmental conditions, and will enable MNP quantification using ICP-MS. The characterization will focus on the physicochemical properties of MNPs, including size, polymer type, and surface chemistry. Aim 2: Investigate MNP translocation mechanisms and toxicity using advanced in vitro models. This will include a triculture model of the small intestinal epithelium and human Intestine-on-Chip (IOC) models derived from both healthy and IBD donor organoids. Simulated digestion will replicate real-world exposure conditions, and the effects of MNPs on intestinal toxicity, gene expression, and inflammatory response will be examined. In addition to providing state of the art, transdisciplinary training to a doctoral student, the findings from this research will provide critical data for assessing the risks of MNP ingestion, inform regulatory actions, and open new research avenues in toxicology and epidemiology for this emerging environmental pollutant.

Freeway Park Association

Freeway Park Association seeks funding to support three complementary projects happening in Freeway Park Dec 24-June 25. We will illuminate pathways with heritage tree lighting; illuminate art and create connections with a community festival; and illuminate history with shared stories and educational signage. The projects include 1. Foundational winter lighting for public delight and much needed safety, and to create a backdrop for our March art activation; 2. An illuminated art event in March entitled `Meeting at the Balance` supporting 6-9 artists/artist teams' art installations, performances, and art making workshops; 3. Creating public education materials about the social and political history of the park and the details of the Park's renovation which is slated for May 25. Meeting at the Balance will energize and illuminate the park, empower and fund local artists and also educate the community about the future and past of Freeway Park at this moment of expansion and change.

Andrew W. Mellon Foundation

Grants for museums, performing arts organizations, and cultural institutions advancing humanities and artistic practice.

Memphis Arts Council

Project and operating grants for arts organizations and individual artists from Memphis Arts Council. Supports visual, performing, literary, and media arts.

FIC - John E. Fogarty International Center for Advanced Study in the Health Sciences

Weight gain following initiation of integrase strand transfer inhibitor (INSTI)-based antiretroviral therapy (ART) is a major emerging public health threat, significantly increasing risks for dyslipidemia, systemic inflammation, hypertension, diabetes, and cardiovascular disease among people with HIV (PWH) in both the United States (U.S.) and globally. Addressing this challenge is a priority for U.S. health, as identifying why some individuals experience "excessive" weight gain (well beyond “return to health” weight gain) will enable earlier, targeted interventions in at-risk U.S. populations. This research environment cannot be replicated in the U.S. due to extreme clinical heterogeneity: the U.S. Food and Drug Administration (FDA) has approved 26+ individual ARV medications across 7 mechanistic classes, leading to diverse prescribing patterns in which only ~52% of patients follow recommended initial regimens. Furthermore, the median U.S. ART treatment duration is 9.8 years, creating a complex history of prior drug exposures that act as significant confounders in metabolic studies. In contrast, Nigeria uniquely offers a high volume of new HIV diagnoses and a near-uniform use of TLD (tenofovir/lamivudine/dolutegravir). This uniformity provides a unique "natural laboratory" that yields faster, more direct answers about metabolomic and lipidomic signatures by eliminating the noise introduced by varied drug histories. Consequently, these findings can be scaled and adapted globally, directly benefiting the U.S. by informing next-generation diagnostic tools, treatment strategies, and prevention modalities. We hypothesize that substantial early weight gain on TLD is driven by distinct alterations in metabolic and lipid pathways. To test this, we will: 1) Determine the effect of substantial early weight gain on TLD on insulin resistance, blood pressure, dyslipidemia, and inflammation. We will enroll previously ART-naïve patients who initiated TLD regimens (n=200 total) in northern Nigeria and gained <3% body weight (n=100) versus >10% body weight (n=100) over their first 12–24 months of therapy. 2) Determine the metabolic and lipid pathways associated with weight gain during the first 12 months of TLD exposure using metabolomic and lipidomic profiling. We will enroll 60 ART-naïve patients initiating TLD and collect longitudinal sociodemographic, behavioral, clinical, metabolomic, and lipidomic data, along with abdominal CT imaging, to characterize visceral adiposity, hepatic density, and alterations in carbohydrate and lipid metabolism among participants with differing weight trajectories.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

PROJECT SUMMARY The kinase Akt is a central mediator of insulin signaling. Its activation by insulin occurs when Akt is phosphorylated at two canonical sites, T308 and S473. Other covalent posttranslational modifications also contribute to Akt regulation, such as phosphorylation at alternative residues, acetylation, and ubiquitination. In this grant, we investigate a distinct mechanism of Akt activation: controlled access to a manganese (Mn2+) ion. Mn is an essential trace element that is acquired through the diet and excreted primarily via efflux from hepatocytes into bile. The efflux of Mn is mediated by the canalicular transporter Slc30a10. We have found in mice, cells, and in vitro that increased Mn availability directly promotes Akt activity in hepatocytes, in a manner that does not require upstream insulin signaling. The Mn-induced activation of Akt is sufficient to suppress glucose production, which provides a biochemical explanation for longstanding observations that Mn has glucose-lowering effects in humans and mice. Moreover, we have found that Mn availability is regulated nutritionally, via carbohydrate signaling. In this grant, we will use classic and state-of-the-art biochemical tools to investigate the cellular and biophysical features of the interaction between Akt and Mn. We will furthermore use genetic and dietary interventions in mice to investigate how control over Mn availability contributes to normal physiology and states of overnutrition. Success of this work will reveal a novel mechanism of regulating Akt activity and hepatic glucose production and generate new avenues for research in metabolism and cell signaling.

NIA - National Institute on Aging

SUMMARY Metals are neurotoxic at high doses yet can contribute to motor and cognitive deficits even at environmentally relevant doses. Metals contribute to amyloid β misfolding and tau hyperphosphorylation, which are pathological hallmarks of Alzheimer’s disease (AD) and AD-related dementia (ADRD) risk as well as cognitive decline. Metals also interact with the APOE4 allele to influence AD risk, advance neurodegeneration, and have vascular effects that may further contribute to dementia risk. Metals may thus represent multiple hits for risk of cognitive impairment and dementia. Yet, few cohort studies have comprehensively evaluated the association of metal exposures with mild cognitive impairment (MCI) and AD/ADRD. To fill this knowledge gap, we propose to leverage the NIH-funded Atherosclerosis Risk in Communities (ARIC) and Multi-Ethnic Study of Atherosclerosis (MESA) cohorts of diverse US adults to test the hypothesis that widespread exposure to metals—determined by established and novel biomarkers—is associated with MCI and AD/ADRD risk and with key pathophysiological processes that explain this risk. ARIC and MESA have rich biorepositories, as well as examination, laboratory, omics and clinical data. In these unique and diverse cohorts, we propose to add a metallome profile to quantify metal exposure and internal dose for each participant by measuring metals in urine, blood, and serum at repeated visits in all participants, as well as in brain-derived extracellular vesicles in a subset of participants. Priority metals include lead, cadmium, copper, mercury, manganese and zinc, although other metals will also be measured. We will connect these metallome profiles with rich brain health and multi-omics data (whole genome sequencing, epigenomic/methylomic, transcriptomic, proteomics, targeted and untargeted metabolomics). We will use powerful, state-of-the-art analyses to determine the prospective associations of long-term metal exposures with risk of cognitive decline, MCI and AD/ADRD risk (Aim 1), and with the trajectory of plasma AD and brain imaging biomarkers (Aim 2) in diverse US adults overall and by sex, race/ethnicity, and APOE4 genotype. We will then develop a predictive multi-omics fingerprint that quantifies risk of MCI, AD/ADRD, and cognitive decline due to metal exposures (Aim 3). Because metal exposures are preventable and treatable, adding high-quality measures of the metallome profile to diverse cohorts with longitudinal brain health and extensive omics data will enable this project to contribute key knowledge of the molecular/biological pathways involved in development of cognitive decline as well as identify new targets for the prevention and treatment of AD/ADRD. This work will generate critical knowledge and serve as a robust model for generating highly valuable data that can be leveraged to prevent/mitigate harmful metal exposures and protect cognitive health.

Metcalf Foundation

The Metcalf Foundation supports performing arts innovation, environmental programs, and inclusive local economies in Ontario.