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The Community Foundation of Greater New Haven

The Community Foundation of Greater New Haven ($600M in assets) supports nonprofits in CT through grants focused on education, community development, arts, health. Awards range from $2,500 to $150,000.

The Community Foundation of Herkimer & Oneida Counties

The Community Foundation of Herkimer & Oneida Counties ($200M in assets) supports nonprofits in NY through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

The Community Foundation of Jackson Hole

The Community Foundation of Jackson Hole ($250M in assets) supports nonprofits in WY through grants focused on education, environment, community development, arts. Awards range from $2,000 to $75,000.

The Community Foundation of Louisville

The Community Foundation of Louisville ($500M in assets) supports nonprofits in KY through grants focused on education, community development, arts, health. Awards range from $2,000 to $100,000.

The Community Foundation of Middle Georgia

The Community Foundation of Middle Georgia ($150M in assets) supports nonprofits in GA through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

The Community Foundation of North Texas

The Community Foundation of North Texas ($800M in assets) supports nonprofits in TX through grants focused on education, community development, arts, health. Awards range from $2,500 to $200,000.

The Community Foundation of Palm Beach and Martin Counties

The Community Foundation of Palm Beach and Martin Counties ($300M in assets) supports nonprofits in FL through grants focused on education, health, community development, arts. Awards range from $2,000 to $100,000.

The Community Foundation of South Alabama

The Community Foundation of South Alabama ($200M in assets) supports nonprofits in AL through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

The Community Foundation of Tampa Bay

The Community Foundation of Tampa Bay ($500M in assets) supports nonprofits in FL through grants focused on education, community development, arts, health. Awards range from $2,000 to $100,000.

The Community Foundation of Western Connecticut

The Community Foundation of Western Connecticut ($150M in assets) supports nonprofits in CT through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

The Community Foundation of Western Massachusetts

The Community Foundation of Western Massachusetts ($300M in assets) supports nonprofits in MA through grants focused on education, community development, arts, health. Awards range from $1,000 to $75,000.

The Dallas Foundation

The Dallas Foundation ($500M in assets) supports nonprofits in TX through grants focused on education, community development, health, arts. Awards range from $2,500 to $150,000.

The Dayton Foundation

The Dayton Foundation ($500M in assets) supports nonprofits in OH through grants focused on education, community development, health, arts. Awards range from $2,000 to $100,000.

NHLBI - National Heart Lung and Blood Institute

Project Summary Atrial fibrillation (AF) is a major cause of morbidity, stroke and mortality affecting 2-5 million Americans. Recent trials have revolutionized the field, by showing that treating patients classified early in their AF process with anti-arrhythmic strategies can reduce morbidity and increase survival versus treatment with rate control medications. Unfortunately, current definitions of `early AF' are highly inconsistent, so that many patients may be excluded from rapid therapy while others may be treated who are unlikely to benefit. This proposal focuses on developing novel computational phenotypes for patients with early stage atrial fibrillation. This proposal builds on preliminary data from our last funded cycle, novel tools we have developed and datasets we have curated in thousands of AF patients. Aims 1 and 2 will develop computational phenotypes for various forms of early stage AF, which address actionable clinical treatment with non-interventional or ablation therapy. For this, we will develop state-of-the-art machine learning models that we apply to very large datasets from our medical records. For Aim 2, we will integrate body surface mapping, imaging and rich clinical data. We will test models in independent cohorts to test the generalizability of our results across populations. Aim 3 will test models prospectively in a pilot study. Our studies address academic rigor, specifically including a broad range of patients, and we will study sex as a biological variable. This study will deliver immediate clinical and translational impact, accelerating personalized medicine for patients with AF. Results from the project will enable clinicians to classify patients with early-stage AF that are amenable to therapy, versus forms of AF which are less amenable. The project will provide translational insights which could inform future mechanistic studies. We will develop unique datasets and novel computational tools which we will share with the research community through our github and established Institutional portals. Our multi-disciplinary team comprises experts in electrophysiology, imaging, computer science, artificial intelligence and biostatistics. The proposal is thus highly feasible.

NIMH - National Institute of Mental Health

Summary There is an urgent need for objective and robust diagnostic indices related to psychiatric illnesses, including obsessive-compulsive and anxiety disorders. Brain-based indices are particularly suited for this purpose, but many of the available brain-based markers have limited scope, require specialized equipment, or have unknown reliability and validity. The proposed research aims to examine the value of data-based, quantitative, and objective markers of dysfunctional electrocortical processes associated with obsessive-compulsive and anxiety psychopathology. The proposed research aims to establish advanced computational indices based on resting electroencephalogram (EEG) recordings that are capable of (1) discriminating between diagnostic categories but also (2) predict transdiagnostic variables such as severity and comorbidity. Specifically, we use state-of-the- art data transformations to extract mechanistically informative indices of spectral shape and alpha-frequency phenomena inherent in EEG recordings during resting states. We will then establish their reliability and internal consistency—prerequisites for using them as markers of inter-individual differences. The indices will then be related to clinical data collected in a large sample of individuals presenting with symptoms on the obsessive- compulsive and anxiety spectrum. A Bayesian Hierarchical Model will be used to aid in data reduction and to measure and heighten reliability of the EEG-derived variables. Finding reliable and valid biomarkers of electrocortical processes has the potential of transforming diagnostic assessment by providing continuous indices of cortical dysfunction. If the goals of this application are met, then reliable and valid indices of electrocortical (dys)function may help to significantly shift clinical practice: In assessment, objective measures of EEG alpha reactivity could be used, for example, to objectively identify patients with perception/attention dysfunction, versus those with generally delayed oscillatory activity and thus more general cortical dysfunction. These inter-individual differences may in the future guide how patients are assigned to individualized treatment protocols as well as for predicting treatment outcome.

The Feels

The Feels Annual Showcase brings diverse creatives and communities together as a safe, inclusive experience. The art exhibit, vendor market, panel discussion and live musical show will be a one-day event on February 23rd from 6pm to 10pm at AXIS Pioneer Square located at 308 1st Ave S Seattle WA. The event will also stream online.

The Foundation for the Carolinas

The Foundation for the Carolinas ($2.7B in assets) supports nonprofits in NC through grants focused on education, community development, arts, health, environment. Awards range from $5,000 to $250,000.

The Greater Cedar Rapids Community Foundation

The Greater Cedar Rapids Community Foundation ($200M in assets) supports nonprofits in IA through grants focused on education, community development, health, arts. Awards range from $1,000 to $50,000.

The Greater New Orleans Foundation

The Greater New Orleans Foundation ($400M in assets) supports nonprofits in LA through grants focused on education, community development, health, environment, arts. Awards range from $2,000 to $100,000.

The Greater Saint Louis Community Foundation

The Greater Saint Louis Community Foundation ($500M in assets) supports nonprofits in MO through grants focused on education, community development, arts, health, racial equity. Awards range from $2,500 to $150,000.

The Greater Tacoma Community Foundation

The Greater Tacoma Community Foundation ($300M in assets) supports nonprofits in WA through grants focused on education, community development, health, arts. Awards range from $2,000 to $75,000.

NHLBI - National Heart Lung and Blood Institute

DESCRIPTION (provided by applicant): Heart failure (HF) is a prevalent healthcare concern associated with unacceptably high mortality rates and significant decreases in quality of life. Chronic inflammation contributes to HF pathogenesis; however, the precise role of the immune response during disease is not fully understood. Acute pressure overload, imposed in the mouse by transverse aortic constriction surgery (TAC), evokes a strong local inflammatory response. Signals emitted from stressed cardiomyocytes trigger the inflammatory cascade and cardiac expression of proinflammatory cytokines and chemokines increases. While most immune-targeting therapies have shown attenuating effects on HF after TAC, depletion of macrophages promoted functional decline, suggesting there may also be beneficial effects from the inflammatory response. One macrophage-derived cytokine that might have favorable effects during HF is meteorin-like (METRNL). METRNL is secreted by myeloid cells and was shown by our group to have a proangiogenic effect after myocardial infarction by binding to the KIT receptor on endothelial cells (ECs). The interaction between METRNL-producing inflammatory cells and KIT+ ECs is a prime example of the importance of paracrine communication in tissue repair after heart injury and opens up a new therapeutic approach. Considering that myeloid cells swiftly accumulate in the pressure-overloaded myocardium and may release protective factors, and that myocardial angiogenesis helps preserve heart function during persistent afterload stress, we hypothesize myeloid cell-derived METRNL may play an important, adaptive role in this context. This proposal aims to investigate the beneficial aspects of inflammation in HF by defining, specifically, the role of METRNL and its receptor, KIT, after pressure-overload. We want to determine if METRNL is involved in the pathogenesis of HF and assess its use as a therapy for disease amelioration. Our preliminary work supports that METRNL attenuates pressure overload-induced HF. Metrnl and Kit transcriptional expression increase significantly following TAC, and Metrnl-deficient mice have reduced survival and heart function after TAC. Our preliminary data show that patients with severe aortic stenosis have elevated METRNL plasma concentrations, indicating pressure overload also triggers METRNL release in humans. We will use genetic gain- and loss-of-function approaches to study the role of myeloid cell-derived METRNL and its receptor KIT in the pressure-overloaded heart. Our goal is to elucidate the role of METRNL in regulating HF progression (Aim 1), to define the major cell types producing and targeted by METRNL (Aim 2), and to assess METRNL’s therapeutic potential in HF (Aim 3). Successful completion of these aims will shed light on the role of crosstalk between the immune system and heart tissue during HF, and evaluate potential protein and gene transfer-based therapeutic approaches for attenuating disease progression. Our work plan and the state-of-the-art research environment emphasize technical and nontechnical training in skills that are highly relevant in contemporary cardiovascular research. The envisioned training will efficiently prepare me for a career as an independent scientist.

Magnolia Chamber of Commerce

This grant will fund Phase 2 of the Magnolia Chamber of Commerce mural project that was developed during 2017 with a 2017 NMF award. The mural project will enhance Magnolia Village's downtown core by painting a vibrant, interactive mural integrating art designs from neighbor school children, with a culminating community celebration event. The content of the mural is based on representing groups of three different species birds flocking together: A visual metaphor of innovative collaboration and interaction that many parts make a whole.

NCI - National Cancer Institute

Project Summary Somatic mutations of PHF6 are common in diverse hematologic malignancies, including T-cell acute lymphoblastic leukemia (T-ALL, 15%), mixed phenotype acute leukemia (MPAL, 23%), acute myeloid leukemia (AML, 3%), chronic myelomonocytic leukemia (CMML, 5%), and myelodysplastic syndrome (MDS, 3%). PHF6 mutations confer worse overall survival in AML and MPAL. Despite the clinical significance, the molecular mechanisms underlying PHF6 mutation mediated leukemogenesis remain to be explored. The PHF6 genetic lesions in hematological malignancies are largely frameshift and nonsense. The PHF6 gene is located on the X chromosome, and its mutation was thought to be a loss-of-function mutation. However, Phf6 D/D mice do not develop spontaneous hematologic malignancies. A recent study (Ahmed et al. Hum Mol Genet 2023) and our preliminary data showed that truncated PHF6 proteins were detectable in blood cells from three BFLS patients and an HPB ALL cell line with PHF6 truncation mutations. Furthermore, while PHF6 mutations were originally reported predominantly in male T ALL patients, subsequent studies from multiple independent groups have failed to show such a biological sex preference. All these data led us to hypothesize that the truncated PHF6 may exert gain-of-function, in addition to a loss-of-function, in leukemogenesis. We thus generated patient derived mutant Phf6 transgenic (Phf6R274XTg and Phf6R342XTg) mouse models by expressing truncated FLAG-PHF6aa1-273 or -PHF6aa1-342 protein in the hematopoietic lineages. Unlike Phf6 D/D mice, Phf6R274XTg mice and Phf6R342XTg mice developed a spectrum of spontaneous hematologic malignancies, recapitulating the characteristics of PHF6-mutated hematologic malignancy patients. Our goal is to decipher the molecular mechanisms through which the PHF6aa1- 273 leads to leukemogenesis. Three specific aims are proposed. Aim 1: Characterize the hematologic malignancies driven by truncation of PHF6 expression in vivo; Aim 2: Decipher the molecular mechanisms by which truncation of PHF6 expression leads to leukemogenesis; and Aim 3: Explore the therapeutic potential of targeting the truncation of PHF6-enhanced KAT6A/B activity in hematologic malignancies. Our newly generated mouse models, state-of-the-art epigenetic assays, and our collaborative team with longstanding expertise in HSPC biology and hematologic malignancies offer us cutting-edge platforms to successfully carry out the proposed studies. Successful completion of the proposed studies will fill a knowledge gap of the molecular mechanisms underlying PHF6 mutation-mediated hematologic malignancies, which will be pivotal for identifying novel therapeutic targets (s).