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The Montana Community Foundation

The Montana Community Foundation ($150M in assets) supports nonprofits in MT through grants focused on education, environment, community development, arts. Awards range from $1,000 to $50,000.

National Institutes of Health

<p style="margin-left:0px;">The National Institute of Diabetes and Digestive Diseases and Nutrition (NIDDK) seeks to advance its mission by continuing the work of the NIDDK Gastroparesis Consortium (GpCRC) but also to expand its scope. The collaborative efforts of the GpCRC provided a large database, the Gastroparesis Registry, which is located in the NIDDK central repository and contains information on patients with symptoms of either delayed or normal gastric emptying. It also houses the first U.S. registry of children and adolescents with gastroparesis. The GpCRC provided clarity and insight that set the stage for transforming our understanding of gastroparesis and laid out a road map for approaching other disorders of gastrointestinal (GI) motility. The findings from clinical studies and trials clearly demonstrated that the clinical burden of gastroparesis is significantly greater than previously realized and involves much more than the stomach. Importantly, the underlying mechanisms remain unclear.&nbsp;&nbsp;</p><p style="margin-left:0px;">&nbsp;</p><p style="margin-left:0px;">Interoception is the ability of the nervous system to sense, interpret and coordinate signals from various bodily systems including the GI tract. Many functional GI disorders are associated with a spectrum of overlapping symptoms including nausea, vomiting, and altered bowel habits all of which involve altered interoceptive signaling. This initiative would broaden the scope beyond gastroparesis to include other adult and pediatric GI conditions associated with impaired interoceptive processing to form a Disorders of Gastrointestinal Interoception Consortium (DGIC). The consortium may include up to 6 Clinical Research Centers (described in a companion notice) and a Scientific Data Research Center (SDRC).&nbsp; &nbsp;There would be an emphasis on multidisciplinary approaches that would reveal the underlying mechanisms that connect GI function more directly to symptoms, identify disease or response biomarkers that assess treatment efficacy, and leverage state-of-the-art technologies to identify novel therapeutic targets that could be assessed in future clinical trials. The SDRC will coordinate collaboration among the Clinical Research Centers, participant enrollment, biospecimen collections and processing, and manage the submission of data and samples to central databases and repositories.&nbsp; &nbsp;</p>

National Institutes of Health

The National Institute of Diabetes and Digestive Diseases and Nutrition (NIDDK) seeks to advance its mission by continuing the work of the NIDDK Gastroparesis Consortium (GpCRC) but also to expand its scope. The collaborative efforts of the GpCRC provided a large database, the Gastroparesis Registry, which is located in the NIDDK central repository and contains information on patients with symptoms of either delayed or normal gastric emptying. It also houses the first U.S. registry of children and adolescents with gastroparesis. The GpCRC provided clarity and insight that set the stage for transforming our understanding of gastroparesis and laid out a road map for approaching other disorders of gastrointestinal (GI) motility. The findings from clinical studies and trials clearly demonstrated that the clinical burden of gastroparesis is significantly greater than previously realized and involves much more than the stomach. Importantly, the underlying mechanisms remain unclear. Interoception is the ability of the nervous system to sense, interpret and coordinate signals from various bodily systems including the GI tract. Many functional GI disorders are associated with a spectrum of overlapping symptoms including nausea, vomiting, and altered bowel habits all of which involve altered interoceptive signaling. This initiative would broaden the scope beyond gastroparesis to include other adult and pediatric GI conditions associated with impaired interoceptive processing to form a Disorders of Gastrointestinal Interoception Consortium (DGIC). The consortium may include up to 6 Clinical Research Centers (described in a companion notice) and a Scientific Data Research Center (SDRC). There would be an emphasis on multidisciplinary approaches that would reveal the underlying mechanisms that connect GI function more directly to symptoms, identify disease or response biomarkers that assess treatment efficacy, and leverage state-of-the-art technologies to identify novel therapeutic targets that could be assessed in future clinical trials. The SDRC will coordinate collaboration among the Clinical Research Centers, participant enrollment, biospecimen collections and processing, and manage the submission of data and samples to central databases and repositories.

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.

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.

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.

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.

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.

European Commission - HORIZON

Towards a fair and transparent market for cultural and creative content in the era of generative AI. Call: Culture, Creativity and Inclusive Society 2026. Programme: HORIZON. Keywords: Artificial intelligence, intelligent systems, multi agent systems, Business models, Copyrights, Data and image processing, Experimentally-driven research and innovation, High performance computing, Information systems, Machine learning, statistical data processing and applications using signal processing (e.g. speech, image, video), Trustworthy ICT, Visual arts, performing arts, design. Open call from the EU Funding & Tenders Portal.

NIGMS - National Institute of General Medical Sciences

Project Summary Signals that cells receive over time from a small set of pathways (e.g., BMP, Wnt, and TGFβ) shape their fate and phenotype during development, regeneration, and disease. Despite their central importance, signaling histories of individual cells are often inaccessible to direct observation, hindering quantitative analysis and obscuring their connection to eventual cell fate. This challenge is particularly pronounced in mammalian systems, where limited optical access and the constraints of size and timescale often render live imaging impractical. To address this issue, we have developed an approach to reconstruct the history of signaling activity in single cells based on endpoint fluorescence images. This is achieved by regulating CRISPR base editors to generate mutations in engineered target sites at rates proportional to the signal of interest. These mutations create a heritable record of signaling activity in the genome, which can be read out at a later time, together with the gene expression profile of the cells. Using this approach, we demonstrated that cells retain a memory of their past response level to BMP signaling for up to 18 days, providing a mechanism for long-term interactions between signals that can facilitate coordination of developmental processes over time. In this proposal, we will expand the scope and utility of our signal recording approach by extending its dynamic range to capture the broad spectrum of in vivo signal intensities and enabling simultaneous recording of the sequence and timing of two signaling pathways. We will also engineer mouse embryonic stem cells to record three key developmental pathways: BMP, Wnt, and Nodal. This will allow us to generate stem cell-derived embryo models and chimeric embryos to link cell fate and spatial organization at the onset of organogenesis with signaling activity at different time windows earlier in development. Additionally, we will investigate mechanisms that enable long-term changes in BMP responsiveness following an initial stimulation, without requiring differentiation. We will then test whether similar mechanisms exist in Wnt and Nodal pathways and assess their role in mediating long-term crosstalk between pathways. To achieve these goals, we will take an interdisciplinary approach combining gene editing, quantitative imaging, epigenomic assays, computational analysis, and generation of developmental models. The proposed goals build on my prior publications, recent preliminary data from our lab, and collaborations I have established since launching my lab. This research program will substantially advance the state of the art in molecular recording, transforming it into a technology that can be used in vivo, in mammalian systems to drive biological discovery. Our long term vision is to identify how signaling history controls cellular decision making during development, and how instructions that cells receive are coordinated over time to produce tissues with the correct number, types, and spatial arrangement of cells. Ultimately, this knowledge will inform strategies for tissue engineering, and open new avenues for understanding and treating diseases driven by dysregulated signaling.

NIDA - National Institute on Drug Abuse

Summary/Abstract People with HIV (PWH) remain vulnerable to central nervous system complications (e.g., neurocognitive impairment) despite antiretroviral therapy (ART) that suppresses viral replication. While many etiologies of these complications exist, mitochondrial dysfunction and inflammation are consistently implicated yet seldom studied simultaneously. PWH also use cannabis more frequently than the general population and recent evidence by our group and others indicates that cannabis may protect PWH from mitochondrial damage by improving metabolic homeostasis and reducing inflammation through triggering receptor expressed on myeloid cells (TREM) 2. Moreover, this mechanism may be more important as PWH age, with the average age of PWH currently being >55. This proposed multidisciplinary, translational project will combine a clinical observational study with cellular and in vivo preclinical models to determine the effects of cannabis use on TREM2-mnediated changes in mitochondrial function in the brain in PWH. The preclinical models will include a) personalized ex vivo/in vitro modeling of mitochondrial toxicity in brain macrophages and neurons, and b) a mouse model for HIV-induced neurotoxicity (Eco-HIV) and age-related neuropathogenesis (TREM2*R47H). Using this multilevel approach, we will test the hypothesis that cannabis effects on TREM2-mediated changes in brain mitochondrial homeostasis vary based on patterns of use: moderate use will be associated with beneficial effects, due to the TREM2 promoting and anti-inflammatory properties of cannabis, but chronic daily use will have detrimental effects. In a cohort of aged (>50 years old) PWH across a range of cannabis use from naïve to daily users, we will measure in plasma and cerebrospinal fluid (CSF) a panel of biomarkers that reflect the mitochondrial homeostasis, TREM2 function, and inflammation. These readouts will be correlated with neurocognitive assessments and PET imaging for TSPO, a marker of neuroinflammation associated with mitochondrial function (Aim 1). We will model brain macrophages using personalized ex vivo cultures of monocyte derived microglia collected from Aim 1 study participants and culture these cells with neurons to identify mechanisms of mitochondrial dysfunction (Aim 2). Using a cross-species approach, we will investigate how different precise doses of cannabinoids interact with HIV and TREM2 variants to affect mitochondrial homeostasis in wild-type and TREM2*R47H mice infected with EcoHIV (Aim 3). This highly innovative, multidisciplinary research proposal is very likely to generate impactful translational knowledge regarding mechanisms of pathogenesis and guide future therapeutic interventions. With our combined clinical and pre-clinical expertise in HIV infection, substance abuse, imaging, and mitochondrial homeostasis, we are uniquely suited to perform the proposed research.

Triangle Community Foundation

Triangle Community Foundation ($600M in assets) supports nonprofits in NC through grants focused on education, community development, arts, environment. Awards range from $2,500 to $150,000.

Tulsa Community Foundation

Tulsa Community Foundation ($4.5B in assets) supports nonprofits in OK through grants focused on education, arts, social services, community development. Awards range from $2,500 to $250,000.

U.S. Mission to Colombia

PAS Bogota invites proposals for programs that strengthen societal and cultural ties, shared values, and bilateral cooperation between the United States and Colombia in support of U.S. Embassy Strategic Goals. All programs must include a U.S. cultural or educational element or connection with American expert/s, organization/s, or institution/s in a specific field that will promote increased understanding of U.S. policy and perspectives, and build partnerships between our citizens. Examples of PAS Small Grants Program programs include, but are not limited to: Academic and professional lectures, seminars and speaker programs; Artistic and cultural workshops, joint performances, and exhibitions; Awareness-raising programs on the challenges persons with disabilities face accessing the democratic process, including the lack of reasonable accommodations and information to exercise their political rights. Cultural heritage conservation and preservation programs; Policy advocacy programs that promote and advance the human rights of historically underserved and marginalized groups such as Afro-Colombians, Indigenous, lesbian, gay, bisexual, transgender, queer, and intersex (LGBTQI+), persons with disabilities, and persons otherwise adversely affected by persistent inequality. Workshops to strengthen networks of U.S. government (USG) programs alumni, CSO/NGO networks, entrepreneurial networks, and/or educational groups. Priority Program Areas: The Embassy s Cultural and Educational Grants Program supports U.S. Mission Bogota s strategic objective of enhancing opportunities for citizen participation in support of peace through cultural and educational program and advances the diversity, equity, inclusion, and accessibility (DEIA) and climate and environment priorities. Diversity, Equity, Inclusion, and Accessibility (DEIA) Disability Rights: o Projects that advance the rights of persons with disabilities, build capacity of organizations that advocate for enforcement and effective implementation of disability-inclusive legislation and policies, and promote democracy and political participation of persons with disabilities, among others. o Projects focused on improving access to educational opportunities for persons with disabilities. LGBTQI+: o Policy advocacy programs that advance the rights of lesbian, gay, bisexual, transgender, queer, and intersex (LGBTQI+) persons, including efforts to safeguard LGBTQI+ youth from harmful practices (e.g., so called conversion therapy ). o Programs that improve the quality of investigative journalism and transparency, increase awareness of the impact of stereotypical and biased reporting on LGBTIQI+ persons and women, and help counter disinformation. Climate and Environment Environmentally-focused activities addressing the climate crisis, combating wildlife trafficking, fostering resilience, conserving nature, water security, and reducing harmful pollutants, including, but not limited to, awareness raising campaigns, leadership, or capacity-building training workshops for youth and underserved communities, a recycled art installation or competition, among others. In addition to the outlined priority program areas, the Public Affairs Section may give consideration to project proposals focusing on the following topics: Science, Technology, Engineering, Arts, and Mathematics (STEAM) Economic empowerment of women, girls, Afro-Colombians, Indigenous communities, the Venezuelan diaspora, LGBTQI+ persons, and other underserved populations. Any other initiatives supporting Colombia s transition to a sustainable and inclusive peace. Project proposals managed by teams of U.S. government (USG) program alumni or designed to strengthen the USG alumni network in Colombia are highly desirable and will be given priority.