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The Pittsburgh Foundation

The Pittsburgh Foundation ($1.5B in assets) supports nonprofits in PA through grants focused on education, community development, health, arts, environment. Awards range from $5,000 to $200,000.

Power of Rage

A one-day event highlighting art, entertainment and food, including an indoor street fair will be held on Sunday March 8, 2020 at historic Washington Hall, 153 14th Avenue from 10:00 am - 6:00 pm. The program will feature local performers, visual artists, artisans, informational tabling from community organizations, and culinary delights provided by local pop-up restaurant chefs. This event is intended to promote acceptance of cultural, social, physical and racial differences while promoting civic participation.

NHLBI - National Heart Lung and Blood Institute

PROJECT SUMMARY/ABSTRACT Heart failure (HF) is a leading cause of mortality worldwide. The metabolism of the failing heart is commonly characterized by increased glucose uptake, glycolytic dependence, and reduced oxidative phosphorylation. We previously demonstrated that blocking glucose oxidation is sufficient to cause hypertrophy and subsequent HF. Additionally, our preliminary data shows that an altered pyruvate-lactate metabolic axis may be pivotal in human HF. Research investigating both the mechanistic regulation and biological roles of the pyruvate-lactate metabolic axis in cardiac metabolism during HF and cardiac recovery is warranted and also has the potential to identify novel druggable pathways to target for future pharmacological approaches. The overall objective of this application is to test the hypothesis that impaired pyruvate oxidation is a cardinal feature of HF in humans and animal models and that myocardial recovery is tightly coupled to normalization of the pyruvate-lactate metabolic axis. We will quantify the pyruvate-lactate metabolic axis in human HF and myocardial recovery (Aim 1). Next, we will determine the essentiality of the pyruvate-lactate metabolic axis for HF and cardiac recovery (Aim 2). Lastly, we will define cell-autonomous mechanisms that regulate the pyruvate-lactate axis in HF and recovery (Aim 3). These experiments will allow us to identify patterns of metabolic alteration in the pyruvate-lactate axis and molecular pathways during HF and myocardial recovery. Understanding the role of pyruvate and lactate metabolism in HF and myocardial recovery is cutting-edge research. Our unique access to human HF myocardium from patients administered stable isotope-labeled glucose or lactate to quantitate pyruvate metabolism in HF and recovery is state-of-the-art and will likely help us reveal new fundamental mechanisms of cardiac metabolism and expedite the successful translation of therapeutics being validated in various models of HF and recovery.

NIGMS - National Institute of General Medical Sciences

Project Summary Modern genome sequencing has shown that many species exchange genes with their close relatives through a process known as hybridization. As a result, the genomes of modern species are a mosaic of regions derived from past hybridization. Because of this, many species including our own must contend with the potentially negative consequences that can arise from mixing two divergent genomes. One of these negative consequences is the exposure of “hybrid incompatibilities” or genes that do not interact properly in hybrids. Uncovering the evolutionary forces that drive the formation of these hybrid incompatibilities is crucial to understanding how the genomes of modern species function. Although this is an important question, we have rarely been able to identify the genetic architecture of hybrid incompatibilities in vertebrates and lack the empirical data needed to understand what predisposes certain genes or genomic regions to negative interactions in hybrids. My postdoctoral research will investigate the evolution of a repeatedly evolved hybrid incompatibility in fish species where hybrid offspring from multiple crosses develop melanoma. I will combine classical genetic crosses, population genomics, and state-of-the-art functional genomic techniques to generate a comprehensive model of how hybrid incompatibilities evolve. In Aim 1, I will perform multiple genetic mapping crosses to identify genomic regions that drive hybrid melanoma. In Aim 2, I will characterize structural variation in the genome and its functional consequences on pigmentation genes involved in hybrid melanoma. Finally, in Aim 3, I will complement this work with a comparative genomic and transcriptomic approach to investigate how genes controlling pigmentation function within gene regulatory networks and become disrupted in hybrids with melanoma. Together, these approaches will give us unprecedented insights into how hybridization has shaped our genomes and the repeated origin of an evolutionarily and biomedically important phenotype. My primary goal under this NRSA F32 fellowship is to receive the scientific and professional training I need to establish my own independent research lab that unites molecular and computational biology with cutting-edge genomic approaches to establish models for how evolutionary processes shape genome content and function. As a postdoctoral fellow in the Schumer and Petrov labs at Stanford University, I will receive training in cutting-edge genomic techniques and analytical approaches. In addition to my scientific training, I will strengthen the professional skills needed to establish my future lab including grantsmanship, network building, and mentorship. In sum, with the training I will receive under this fellowship, I will be poised to lead a research program with great power to link molecular mechanisms to evolutionary outcomes and connect genotypes to phenotypes at the molecular and organismal level.

NIDDK - National Institute of Diabetes and Digestive and Kidney Diseases

Project Summary/Abstract: This NRSA proposal, tailored to Ms. Hibbard, provides high-quality predoctoral research training and career development centered upon her future goals. The sponsor’s excellent mentoring record, collaborations with leading biomedical researchers, and the outstanding environment at the IUSM and Indiana Center for Musculoskeletal Health (ICMH) will foster the successful completion of this project. Additionally, participation in the Preparing Future Faculty and Professionals program for ethics and grant writing courses, manuscript preparation, departmental seminars and journal clubs, as well as national meetings will enhance Ms. Hibbard’s career development towards becoming a well-rounded, independent investigator. Patients with chronic kidney disease (CKD) develop renal fibrosis, which is a common pathological manifestation of virtually all etiologies of CKD, and one of the major causes of end-stage renal failure. Currently, there are no direct therapies for this manifestation. My preliminary data demonstrate that fibroblast activation protein (FAP) is highly expressed in CKD kidney, and our initial RNAseq datasets support that FAP is associated with altered myofibroblast motility and matrix composition. Thus, our models of the interactions between fibrosis and the effects of FAP on this patient phenotype remain incompletely understood. The primary goal of the present application is to test new hypotheses regarding drivers of CKD fibrosis, including FAP as well as its direct targeting in pre-clinical studies. Although my initial results show increased Fap mRNA and protein in the kidney of mice with CKD, the effects of targeting FAP to reduce renal fibrosis, are unstudied. Thus, the central hypothesis is: FAP increases renal fibrosis onset and progression in CKD through enhancing matrix secretion and cell migration, and CD5/LNP-FAPCAR will target FAP+ activated fibroblasts to reduce pathologic CKD outcomes. In Aim 1, the role of Fap in progression of CKD fibrosis will be tested using FAP-KO mice, and in isolated cell culture studies. Aim 2 will test the translational, pre-clinical rescue of renal fibrosis during CKD using a novel targeted anti-fibrotic therapy and scRNAseq. By performing these studies, Ms. Hibbard will gain new research skills in utilizing state-of-the-art translational mouse models, bioinformatic skills, and CKD treatments. Collectively, this proposal will also provide excellent research, ethics, and written and oral presentation training to Ms. Hibbard, as well as test important disease mechanisms that result in kidney fibrosis, and its potential resolution.

NIA - National Institute on Aging

PROJECT SUMMMARY/ABSTRACT Background: Aging is associated with reduced muscle mass and physical function, which may be exacerbated by age-associated diseases including peripheral artery disease (PAD). PAD affects about 8-12 million individuals in the United States and an estimated 10-15% of the population age ≥65. In PAD, skeletal muscle (SkM) metabolic dysfunction contributes to physical limitation and mobility disability. Few therapies have been identified that improve walking impairment in people with PAD; thus, therapeutic interventions targeting the pathophysiology of the SkM metabolic myopathy are promising. MicroRNAs (miRs) are powerful regulators of gene expression, specifically in the context of energy metabolism. MiRs have great potential as therapeutic agents due to the ability of a single miR to regulate entire pathways. In my preliminary studies, I found that miR-1, the most abundant miR in SkM, appears to play a critical role in hindlimb ischemia models and in human PAD. I developed a genetically modified mouse model for inducible, SkM-specific knockout of miR-1 and found that loss of miR-1 results in metabolic inflexibility and compromised running performance. Utilizing state-of-the-art experimental approaches (Argonaute (AGO) enhanced crosslinking and immunoprecipitation, coupled with high-throughput sequencing (eCLIP-seq)), I identified dysregulation of the pyruvate metabolic pathway as a mechanism for reduced SkM oxidative metabolism with miR-1 loss. Proposed Research: The purpose of this proposal is to define the miR-1 regulated transcriptome and investigate how miR-1 and miR-1 target genes contribute to SkM metabolic myopathy and mobility limitation in experimental PAD as well as in the clinical disease. Aim 1 will identify whether rescuing SkM miR-1 expression will ameliorate ischemic pathology. Aim 2 will determine the role of miR-1 in exercise training adaptations in hindlimb ischemia. Aim 3 will assess miR:target binding in PAD samples to determine pathophysiologically relevant mechanistic targets. Together, these Aims will define the miR-regulated transcriptomic response in PAD and will provide a foundation for the development of miR-based therapeutics aimed at SkM metabolism in PAD. Candidate: I have led projects that investigated several aspects of PAD pathophysiology. I have also led studies that explored miRs in SkM through various novel approaches and technologies. This expertise and my established track record in working with transgenic mouse models will ensure the successful completion of these aims. I will follow up this work and the associated publications with an R01 proposal focused on the role of post-transcriptional regulatory mechanisms in the exercise response heterogeneity in older participants with PAD. The K22 award will be fundamental as I launch my independent investigator career, offering management and grant writing training, helping to hone my skills as a mentor/PI and establish a long-term funded research program.

NIAAA - National Institute on Alcohol Abuse and Alcoholism

ABSTRACT Alcohol use disorder (AUD) is a highly prevalent, chronic, relapsing disorder for which pharmacological treatments remain few. People affected by AUD show heavy, compulsive alcohol drinking, a negative emotional state when abstaining from alcohol, and an inability to reduce or stop intake. Key neuroadaptations induced by chronic alcohol include the recruitment of stress neurotransmitter systems in the bed nucleus of the stria terminalis (BNST). The BNST is a brain region that plays a key role in both excessive drinking and anxiety-like behavior. This project concerns pituitary adenylate cyclase activating polypeptide (PACAP), a neuropeptide particularly abundant in the BNST, which has recently emerged as a master regulator of the stress response. The central hypothesis of this application is that the central PACAP system is a key mediator of heavy alcohol drinking and associated anxiety-like behavior and heightened pain sensitivity. Furthermore, we hypothesize that PACAP acts in the BNST via the stimulation of corticotropin-releasing factor (CRF) neurons. Finally, we hypothesize that PACAP projections from the lateral parabrachial nucleus to the BNST are those mediating the effects. These hypotheses will be tested using well-established animal models of heavy alcohol drinking and affective behavior, combined with state of the art pharmacological, molecular, and viral approaches. This highly translational and mechanistic research will shed light on the role of a key neuropeptide system in heavy drinking and anxiety-like behavior. A deeper understanding of the molecular mechanisms underlying heavy drinking and the neuroadaptations occurring in the extended amygdala neurocircuitry may lead to the discovery of novel therapeutic agents for AUD.

NIH

Significance to VA: Lung cancer (LC) is the leading cause of cancer death for US veterans (USvets). Non-small cell LC (NSCLC) represents the majority of LCs with a poor 5-yr survival rate (~23%). NSCLC patients in the VA Health Care System are increasing as USvets often acquire tobacco addiction during military service fostering a large percentage of high-risk current & former smokers. The lung cancer incidence is also higher in USvets with lower survival rates, and LC is linked to service-connected exposure to carcinogens. Current treatment options for NSCLC are palliative, but have recently evolved with the use of immune checkpoint inhibitors (ICIs). Unfortunately, the effectiveness of ICIs in NSCLC remains modest with underlying resistance mechanisms elusive. Our research will define these resistance mechanisms and identify potential molecular targets & strategies to target both the NSCLC tumor & enhance ICI efficacy to produce a more durable outcome for USvets. Innovation & Impact: STK11 mutations (mtSTK11) are common in NSCLC and associated with resistance to immune checkpoint inhibitors (ICIs). Our data connected mtSTK11 to a novel dysregulation of caspase 9 (C9) alternative RNA splicing (ARS). Specifically, mtSTK11 NSCLC preferentially expressed C9b, which induces tumorigenesis, and a tumor immunosuppressive microenvironment (TIME) that supports ICI resistance. Genetic removal of C9b sensitized mtSTK11 NSCLC to ICI therapy in a NSCLC mouse model, thus highlighting the potential utility of modulating dysregulated ARS as a therapeutic. Human mtSTK11 NSCLC tumors also presented with the dysregulation of additional ARS events, which our data also support roles in NSCLC tumorigenesis & TIMEs. These data support the hypothesis that dysregulated ARS in mtSTK11 NSCLC modulates tumorigenesis and induces a TIME that promotes ICI resistance. Specific Aims (SAs): To interrogate our innovative hypothesis, we are proposing three specific aims: SA1: Determine the role of ARS events linked to the mtSTK11 oncogenotype in NSCLC tumorigenesis; SA2: Determine the role of specific STK11-regulated ARS events in ICI responses; & SA3: Determine the signaling mechanisms driving dysregulated ARS in mtSTK11 NSCLC. Methodologies: Unbiased “splicomic” analysis in human NSCLC will identify ARS events dysregulated in the mtSTK11 oncogenotype. Once validated for STK11/LKB1-regulation (e.g., by qRT-PCR), their roles in cancer biology will be determined using cells models (e.g., clonogenic potential) and mtSTK11 NSCLC mouse models (e.g., tumorigenesis & ICI resistance). The mechanism of action for specific ARS events will be determined by interrogation of the cell composition of the TIME using multiplex immunofluorescent histology & Aurora flow cytometry. State-of-the-art molecular manipulations (e.g., CRISPR), novel molecular “tools”, and complementary biophysical studies will be employed to modulate specific ARS events in our cellular & in vivo models and determine mechanistic function. Important ARS events and mechanisms will be interrogated in human NSCLC tumors for translational outcomes (e.g., survival, ICI resistance). Path to translation/implementation: Validation of our hypothesis would lead to the identification of new chemical entities (NCEs) that specifically block cancer-related ARS to foster a new generation of therapeutics for NSCLC. These NCEs would have limited toxic side effects: the “Achilles Heel” for some global ARS inhibitors. Additionally, our laboratory has shown that ceramide induction in NSCLC cells will reverse the dysregulated C9 ARS and sensitize cells to standard of care NSCLC treatments. A new ceramide-induction therapy, ceramide nanoliposomes, recently completed a phase I clinical trial (NCT02834611) for solid tumors (e.g., NSCLC) with an excellent safety profile. Thus, our proposed studies will build the molecular, mechanistic, & pre-clinical foundation for the development of new targeted ARS therapeutics and the clinical implementation of combination therapies using both ARS inhibitors & ceramide-induction therapy with ICIs in NSCLC to improve outcomes.

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary. In people living with HIV (PLWH) under antiretroviral therapy (ART), secondary lymphoid organs including lymph nodes harbor latent viral reservoirs, which are a major obstacle to curing acquired immunodeficiency syndrome (AIDS). While follicular helper T cells and follicular dendritic cells in B cell follicles are well studied as viral reservoirs in lymph nodes, recently it has been reported that lymph node CD4+ tissue-resident memory T (TRM) cells also serve as viral reservoirs in PLWH on ART. Our preliminary data demonstrate: 1) fibroblastic reticular cells (FRCs), a type of secondary lymphoid organ stromal cells, generate lymph node CD4+ TRM-like cells from peripheral blood CD4+ T cells; 2) FRC-induced lymph node CD4+ TRM-like cells support HIV-1 latency; and 3) FRCs maintain the survival of CD4+ T cells. However, the following critical aspects remain to be defined: 1) the extent of similarity between FRC-induced CD4+ TRM-like cells and bona fide lymph node CD4+ TRM cells, 2) the capability of FRC-induced CD4+ TRM-like cells to be HIV-1 reservoirs, and 3) the role of FRCs in maintenance of TRM viral reservoirs. Thus, the long-term goal of this project is to elucidate the roles of secondary lymphoid organ stromal cells in viral latency, which is critical to developing a curative strategy for AIDS. The objective of this proposal is to define how FRCs contribute to the generation and maintenance of viral reservoirs. Our central hypothesis is that FRCs facilitate the formation of lymph node CD4+ TRM cells that are highly permissive to HIV-1 latent infection and maintain the survival of latent viral reservoirs. The rationale of the proposed studies is that the completion of the studies will inform about the cellular and molecular mechanisms involved in both the establishment and maintenance of viral reservoirs, as well as possible means of a curative strategy. We plan to test our central hypothesis by pursuing the following three specific aims: In the first aim, we will use single-cell RNA sequencing, single-cell surface phenotyping and DNA sequencing that allows to determine the provirus sequence and phenotype of infected cells at a single-cell resolution, and an in vivo mouse model to establish that FRCs play a role in the generation of lymph node CD4+ TRM cells. In the second aim, to determine the molecular mechanism by which FRC-induced CD4+ TRM-like cells support latent infection, we will focus on a TRM- associated transcription factor and use chromatin immunoprecipitation and immunoprecipitation to define the interactions of the transcription factor with the HIV-1 LTR and host molecules in FRC-induced CD4+ TRM-like cells. In the third aim, we will employ the single-cell surface phenotyping and DNA sequencing that will be used to assess the ability of FRCs to maintain the survival of latently infected FRC-induced CD4+ TRM-like cells containing intact proviruses. This work is innovative because it combines a range of complementary approaches to test a novel hypothesis regarding the roles of FRCs in HIV-1 latency. The proposed research is significant because of the potential to define how latent viral reservoirs are established and maintained in secondary lymphoid organs.

Center for Linguistic and Cultural Democracy

Caribbean culture and arts will be celebrated throughout the summer with a series events including a four week costume making class, cultural workshops at local Caribbean restaurants and a cultural exchange workshop between Jamaica and Ghana highlighting their historic cultural and linguistic ties. The culminating event will be Caribbean Sea Fest on August 13th at Volunteer Park from noon until 8:00 pm. This project highlights the cultural expressions Cuba, Bahamas, Trinidad, Jamaica and Puerto Rico.

The Saint Paul & Minnesota Foundation

The Saint Paul & Minnesota Foundation ($1.2B in assets) supports nonprofits in MN through grants focused on education, community development, racial equity, arts. Awards range from $5,000 to $200,000.

Bronfman Foundation

Supports arts, education, and community development initiatives across Canada with a focus on Jewish community and broader Canadian society.

The San Diego Foundation

The San Diego Foundation ($800M in assets) supports nonprofits in CA through grants focused on education, environment, community development, arts, health. Awards range from $2,500 to $200,000.

Parkview Services

Vibrant Palette, a nonprofit arts program for adults with I/DDS, collaborates with Belltown Arts Walk, The Slide Gallery, and the City of Seattle for 'The Small Things,' an inclusive arts extravaganza. From 1/8/24 through 2/4/24, we will hold workshops and public art viewing. The Small Things provides 3x3 canvases to up to 150 community members, hosts two free in-person workshops, and features an opening event for the displayed art at the Slide Gallery. This project, rooted in accessibility and inclusion, enhances participation in the Seattle arts community for adults with I/DDs.

Soufend Arts Council

The Soufend Arts Council will host a free event to celebrate the creativity, community, and culture of South Seattle. The event will feature an art exhibit, performances, and interactive art activities. It will be held August 24, 2019 from 2 pm - 8 pm on S Holly St between Rainier Ave S and 49th Ave S.

Sustainable Style Seattle

We have an ambitious vision for a "free store" that helps people find clothes they love and re-home clothes they no longer need, all for free. It will provide a much-needed way for people to keep things out of landfill and reform a harmful and exploitative system. The store will also provide a radically inclusive third place that helps people build skills, forge connections, be creative, and support art. We want to be an example of the future of Seattle, one that’s built on innovation, care, dignity, and abundance. This pilot is crucial in changing the narrative of what urban spaces can and should be. We will use the space for the free store and events, but we also want to uplift historically underserved artists by sharing our space. We plan to run for a total of 9 months. We’ll run an initial trial in January, a review and planning period from Feb-Apr, and an extended pilot from May-Sept. We plan to have 1 space, but we’ve had offers to create this concept in multiple spaces.

Belltown Butterflies

The Butterfly Effect—the idea that small actions can have profound impacts—the project invites individuals to tap into their creativity and reflect on how they engage with the world by including art made on small, individual butterflies. At the project's heart is an installation of hundreds of these butterflies made by different community members, symbolizing each person's significance in the fabric of society. Arranged in a flowing chromatic wave, the installation creates an immersive visual experience while fostering connection, self-awareness, and creative empowerment. The installation will be a part of a community art exhibition at Slip and Slide Galleries located at 2301 1st Ave Seattle WA for Belltown Artwalk on Sept 12, 2025, from 6-9 pm. The exhibition will run through Oct 5, 2025. Free and open to all, it enhances accessibility, equity, and public art awareness.

NIAID - National Institute of Allergy and Infectious Diseases

PROJECT SUMMARY/ABSTRACT The University of Texas Southwestern (UTSW) Medical Center is one of the premier academic medical centers in the world and requests support for a new research training program focused on training physician-scientists in the field of infectious diseases. The UT Southwestern Infectious Diseases (UTID) Research Training program will support 2 post-doctoral trainees for a two-year training period every year. The novel design of the UTID training program utilizes cross-campus recruitment for physician scientists working in the field of infectious diseases to create a large pool of candidates. Once recruited, trainees have an extensive interdisciplinary mentorship and a program-specific ID research training program that includes mentors and resources from 9 different departments, divisions, centers, and institutes across the medical campus. The 29 trainers have broad training and are comprised of a core group of highly accomplished, established investigators along with an expanding and impressive group of new and junior faculty mentors that embodies the intradisciplinary research programs across the UTID Training program that are bound by a common interest in combating infectious diseases. The UTID training program serves as an important focus for formal interactions among this overlapping group of talented trainers who have strong records of research success and outstanding records of training physicians and scientists. Our goal is to train post-doctoral physician-scientists for research careers in the molecular basis of microbial pathogenesis, cellular microbiology, host-defense mechanisms, regulation of virulence, structural biology, and clinical research. The research interests of the faculty include bacterial and viral pathogenesis, innate and adaptive immunity, antimicrobial therapeutic discovery, parasitology, RNA biology, and structural biology. The UTID Research Training program provides a strong emphasis on molecular mechanisms, molecular biology, and fundamental quantitative scientific approaches. Trainees who complete the program are expected to apply state-of-the-art molecular approaches to address important current and future problems in the field of infectious diseases. This training program will produce highly trained physician-scientists to address current and future challenges in the field of infectious diseases and immunology. This new program will also provide a pipeline for academic infectious disease research faculty for the region and throughout the US.

The Wichita Community Foundation

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

The Winnipeg Foundation

The Winnipeg Foundation manages a $1B+ endowment and provides grants to strengthen Winnipeg communities through arts, education, environment, health, and social services.

The Winston-Salem Foundation

The Winston-Salem Foundation ($400M in assets) supports nonprofits in NC through grants focused on education, community development, health, arts. Awards range from $2,000 to $100,000.

Toledo Community Foundation

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

Engineering Bureau, Public Works

TOS - Task Order Solicitation

Engineering Bureau, Public Works

TOS - Task Order Solicitation