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Hillsborough County Arts

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

Multimedia Resources and Training Institute (MMRTI)

Multimedia Resources Training Institute will create a 1 hour documentary, 30 photo portraits, and other multimedia projects produced by youth interns.  They will focus on Seattle's Central Area, a Historic Arts and Cultural District. The project will empower youth to act as community advocates through photography and video.

NIAID - National Institute of Allergy and Infectious Diseases

Project Summary HIV drug resistance represents a growing and underappreciated threat to the U.S. HIV response. Although more than 1.2 million people are living with HIV in the U.S., only about 60% achieve durable viral suppression, and resistance is a major contributor to treatment failure and regimen switching. Current resistance testing relies on centralized, PCR and sequencing-based platforms that are expensive, slow, and available only at specialty laboratories, requiring multiple clinic visits and highly trained personnel. As a result, same- day, resistance-informed treatment decisions are rarely possible, even in major U.S. cities, and are essentially inaccessible in rural areas, mobile care units, and safety-net clinics serving areas where the epidemic is increasingly concentrated. These gaps most severely affect communities already carrying the highest burden of HIV incidence and treatment failure in the U.S. Without affordable, accessible, point-of-care (POC) resistance testing, the durability of ART and the success of the national Ending the HIV Epidemic initiative are at risk. Our project aims to develop HIV-CRISP to addresses this critical gap by developing a cost-effective, same- visit “test-and-switch” POC device that integrates CRISPR-based nucleic acid detection with a bioinspired microfluidic chip (CamoChip). This fully automated platform enables simultaneous detection of HIV viral load and drug resistance to four major ART classes (NRTIs, NNRTIs, INSTIs, and PIs) during a single clinic visit. By empowering providers to make immediate, resistance-informed treatment decisions, HIV-CRISP reduces delays in therapy initiation or modification and minimizes the risk of treatment failure. The project is structured around three specific aims: Specific Aim 1: optimize a PAMmer-assisted CRISPR system for accurate detection and profiling of HIV drug resistance mutations; Specific Aim 2: enhance CamoChip readout technology for rapid, multiplex POC testing; and Specific Aim 3: integrate these components into a user-informed POC device and validate its performance against standard methods with clinical samples. Each aim not only drives independent scientific advances but also converges on the development of a transformative POC diagnostic. HIV-CRISP represents an innovation in HIV diagnostics with broad public health significance. This platform supports wide access to high-quality HIV care in under-resourced settings across the U.S. and globally, while also providing a foundation adaptable to other infectious diseases and health conditions.

National Institutes of Health

<p>The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission by supporting four Clinical Trials Networks (CTNs) each comprised of a Leadership and Operations Center, Statistical and Data Management Center, and Laboratory Center (LC) working with Clinical Trials Units, to&nbsp;test&nbsp;prevention and treatment&nbsp;strategies and conduct implementation research designed to end the HIV epidemic. This NOFO will solicit applications for up to four LCs that will provide laboratory structure and technologies to one or more CTNs and conduct laboratory testing for Network trials, according to regulatory standards. The LC oversees site-affiliated clinical and specialized laboratories and ensures protocol-specified laboratory testing.&nbsp; The LC will: 1) support sample integrity from collection to final testing/storage; 2) use appropriate laboratory data capturing management and tracking systems; 3) select, determine readiness, and approve laboratories; and 4) promote state-of-the-art laboratory assays.&nbsp;The LC will increase testing capacity to meet advances in prevention and treatment of HIV and HIV-related diseases.</p><p><br>Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.</p>

National Institutes of Health

The National Institute of Allergy and Infectious Diseases (NIAID) seeks to advance its mission by supporting four Clinical Trials Networks (CTNs) each comprised of a Leadership and Operations Center, Statistical and Data Management Center, and Laboratory Center (LC) working with Clinical Trials Units, to test prevention and treatment strategies and conduct implementation research designed to end the HIV epidemic. This NOFO will solicit applications for up to four LCs that will provide laboratory structure and technologies to one or more CTNs and conduct laboratory testing for Network trials, according to regulatory standards. The LC oversees site-affiliated clinical and specialized laboratories and ensures protocol-specified laboratory testing. The LC will: 1) support sample integrity from collection to final testing/storage; 2) use appropriate laboratory data capturing management and tracking systems; 3) select, determine readiness, and approve laboratories; and 4) promote state-of-the-art laboratory assays. The LC will increase testing capacity to meet advances in prevention and treatment of HIV and HIV-related diseases.Grant authorities that allow NIAID to forecast this opportunity are as follows: Sections 301 and 405 of the Public Health Service Act as amended (42 USC 241 and 284) and under Federal Regulations 42 CFR Part 52 and 2 CFR Part 200.

Hong Kong Jockey Club Charities Trust

One of the world's top charity donors (500M+ USD/yr). Supports youth, elderly, sports, arts, and community programs in Hong Kong.

NIDA - National Institute on Drug Abuse

Project Summary Drug use increases HIV risk and worsens health outcomes in people living with HIV (PLWH). While antiretrovirals are effective for both prevention – using pre-exposure prophylaxis (PrEP) – and for treatment – using antiretroviral therapy (ART) – drug use further impairs medication adherence. It is thus essential to develop strategies to enable people who use drugs to achieve abstinence and prevent relapse, which is expected to reduce HIV risk, burden, and infection. Progesterone and its metabolites regulate drug craving and immune function, making them potential therapeutic targets. However, PLWH and people who use drugs often experience menstrual cycle disruptions, and the impact of PrEP or ART on hormone regulation remains unclear. Understanding these interactions could reveal strategies to reduce drug-seeking behavior and to improve HIV treatment outcomes. In our preclinical work using the EcoHIV mouse model of HIV infection, we observe disrupted estrous cyclicity, altered cytokine expression, and increased risk for cocaine relapse-related behavior. We further observe that ART restores estrous cyclicity and partially reverses altered brain cytokine expression in EcoHIV-infected mice. However, it is unknown whether ART restores cycle regularity in cocaine-exposed, EcoHIV-infected mice or whether PrEP interacts with drug exposure to affect hormonal function. The medial preoptic area (mPOA) regulates both estrous cyclicity and cocaine-related behavior, and our findings suggest EcoHIV infection increases mPOA activation in cocaine-exposed females. Progesterone and its active metabolite, allopregnanolone, act on both neurons and astrocytes. Thus, modulation of mPOA astrocytic and neuronal activity may represent a novel target for reducing drug seeking and neuroimmune dysregulation among those at risk of or living with HIV. This proposal will test the overarching hypothesis that chronic drug exposure and EcoHIV infection interact with antiretrovirals to promote estrous cycle irregularity and cocaine reinstatement via dysregulation of the mPOA. Aim 1 will assess how PrEP and ART impact estrous cyclicity, ovarian reserve, mPOA cellular activity, and neuroimmune signaling following chronic cocaine exposure. Aim 2 will use chemogenetic tools to determine the role of mPOA discrete populations of astrocytes and neurons in cocaine reinstatement after PrEP or ART+EcoHIV. Aim 3 will evaluate whether allopregnanolone administration reduces cocaine reinstatement and alters neuroimmune signaling. Together, these Aims are to expected define the mPOA as a mediator of drug seeking and immune state following treatment with antiretrovirals, and further to identify hormonal strategies to suppress relapse in individuals taking PrEP or with virally suppressed HIV infection.

Houston Endowment

Houston Endowment ($2.0B in assets) supports nonprofits in TX through grants focused on education, arts, environment, community development. Awards range from $5,000 to $400,000.

NIMH - National Institute of Mental Health

ABSTRACT The dynamics of HIV infection in the brain is poorly understood. Infected cells that transport HIV across the blood brain barrier and into the brain causes inflammation and subsequent damage to resident brain cells. This manifests as a group of symptoms collectively referred to as HIV associated neurocognitive deficits (HAND). Today, in the post ART era, HAND consists of mild to moderate symptoms. This research is significant because it uses an in vivo model to assess the unique interactions among brain cells and peripheral immune cells in vivo in an HIV infected ASRT treated model. Results from these studies will give a better understanding of the events that define neuroHIV in the ART era.

IA Arts Council

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

ID Arts Council

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

Idaho Commission on the Arts

Provides general operating support to established Idaho arts organizations for ongoing programming, operations, and capacity building, helping sustain the state's cultural infrastructure.

Idaho Commission on the Arts

The Idaho Commission on the Arts Quick Fund program provides rapid-response grants for arts programming, supporting performances, exhibitions, workshops, and cultural events that bring arts experiences to Idaho communities.

Idaho Community Foundation

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

NCI - National Cancer Institute

Identification and Characterization of Mutation-Induced Alternative Splicing Events in Cancer Using Multi-Omics Data Project Summary The goal of this project is to discover mutation-induced alternative splicing events (MAS), understand their functional relevance, and identify neoantigens arising from these events to advance cancer immunotherapy. Large-scale sequencing efforts such as The Cancer Genome Atlas (TCGA) have primarily focused on identifying driver mutations in tumors, including single amino acid changes, insertions, deletions, and alterations that truncate or elongate wild-type protein sequences. However, traditional DNA mutation annotations often rely on canonical transcripts and may overlook alternative splicing events, and some mutations, such as synonymous changes, are considered silent despite their potential impact on splicing. Previously, we developed the MiSplice pipeline to detect mutation-induced splice sites and, when applied to TCGA data, identified thousands of somatic mutations that create cryptic splice sites. In this proposal, we aim to systematically investigate mutation-induced alternative splicing and its functional relevance in cancer, while also identifying the resulting neoantigens by leveraging data from the Clinical Proteomic Tumor Analysis Consortium 3 (CPTAC-3), which includes comprehensive exome sequencing, RNA-Seq, and mass spectrometry data for 774 tumors across seven cancer types, as well as 126 prospective breast cancer samples from CPTAC-2. We hypothesize that mutation-induced alternative splicing plays a significant role in cancer etiology and that the associated neoantigens can serve as novel immunogenic peptide candidates for cancer immunotherapy. We propose to test these hypotheses through two specific aims. Aim 1: Identify mutation-induced alternative splicing events and assess their functional relevance in cancer using multi-omics data (Years 1 & 2). We will use MiSplice to detect mutation-induced alternative splicing events from CPTAC data and evaluate their impact by analyzing changes in protein and phosphorylation expression, as well as pathway activation. Aim 2: Identify neoantigens arising from mutation-induced alternative splicing events with mass spectrometry support (Years 1 & 2). We will construct a tailored protein database that integrates both reference proteins and mutant proteins generated from MAS events. Using state-in-art tools such as PepQuery, we will search for corresponding peptides in the mass spectrometry data, enabling identification of mutant proteins. Neoantigen peptides derived from these expressed mutant proteins will then be prioritized as candidates for cancer immunotherapy.

NIMH - National Institute of Mental Health

PROJECT SUMMARY/ABSTRACT People with HIV (PWH) who experience challenges with antiretroviral therapy (ART) adherence are at increased risk for suboptimal treatment outcomes, including viral non-suppression and disengagement from care. Despite advancements in ART delivery options, personalized treatment approaches that integrate patient preferences remain underutilized, particularly among PWH facing psychosocial and documented barriers. Clinical decision support (CDS) tools offer a promising avenue to address this gap by tailoring treatment recommendations based on patient-specific needs and barriers. However, current CDS tools often fail to incorporate rich patient insights available from unstructured electronic health record (EHR) notes or systematically integrate directly reported preferences, limiting their potential to enhance adherence and outcomes. The proposed training and research plan for this K23 will enable José I. Gutierrez, Jr., PhD, FNP- BC, to acquire the expertise necessary to become an NIH-funded independent investigator who designs patient-informed CDS interventions that optimize HIV treatment delivery. Under the mentorship of an experienced multidisciplinary team, Dr. Gutierrez will use a mixed-methods approach to develop foundational components of a CDS prototype that integrates natural language processing (NLP)–derived EHR information with patient-reported preference data. Building on prior work in HIV treatment delivery and preference evaluation, he will pursue the following specific aims: (1) explore HIV treatment delivery preferences, barriers, and facilitators within EHR notes using NLP; (2) identify and quantify patient preferences, barriers, and facilitators using qualitative interviews and MaxDiff; and (3) develop the key features of a CDS prototype that generates tailored suggested actions informed by EHR and patient-preference data, and evaluate its acceptability, feasibility, usability, and intended adoption in a 9-month, cross-sectional, non-clinical user-testing study using standardized vignettes and de-identified/fictionalized cases (no live EHR). This research plan aligns with Dr. Gutierrez's career development goal to gain advanced skills in clinical informatics and NLP, qualitative and mixed-methods research, and patient-informed intervention design. Findings will provide the foundation for a subsequent NIH R01 to rigorously evaluate effectiveness in clinical settings, with the overarching goal of improving ART adherence and treatment outcomes among PWH. 1

NCI - National Cancer Institute

PROJECT SUMMARY Oncogenic mutations in KRAS are nearly universal in pancreatic ductal adenocarcinoma (PDAC) and drive disease initiation, progression, and maintenance. Small molecules that inhibit mutant forms of KRAS (KRASi) and both mutant and wildtype RAS proteins (RASi) have recently emerged with the potential to transform the treatment landscape of PDAC. However, the mechanisms dictating efficacy and resistance to RAS inhibitors remain poorly understood. PDAC development and therapeutic response depends on co-evolution and interaction between tumor cells and the tumor immune microenvironment (TIME). This research proposal focuses on a major goal of our laboratories: to determine how remodeling of tumor-immune interactions contributes to efficacy and durability of RAS inhibition. We have developed immunocompetent mouse models that recapitulate seminal features of PDAC heterogeneity and found that while the KRASG12D inhibitor MRTX1133 and the pan-RASGTP inhibitor RMC-6236 both effectively inhibit the MAPK pathway and illicit potent tumor responses in pre-clinical studies, they result in distinct patterns of response and adaptation in tumor cells and the tumor microenvironment. We hypothesize that these differences result from poorly understood and understudied immune cell intrinsic roles of the RAS family that alter interactions between tumor and immune cells in response to RAS inhibition. Using a multidisciplinary and collaborative approach, this proposal integrates cutting-edge genetic models with innovative molecular and immunological methodology to delineate targetable immunological changes which define distinct patterns of response to KRASi and RASi in PDAC. We propose 2 aims that meet the research objectives of notice of special interest NOT-CA-24-016 (Exploratory Cancer Immunology Projects and Technologies (ExCITe)/PA-25-304, by addressing “fundamental aspects of tumor immunology and/or innovative ways to enhance anti-cancer immunity.” Aim 1 will leverage state of the art single cell technology and high dimensional spectral flow cytometry in mouse models of PDAC to comprehensively establish how TIME remodeling contributes to PDAC response and resistance following RASi/KRASi. Aim 2 will investigate immune-intrinsic roles for wild type RAS activity in the PDAC TIME through novel genetic approaches to determine how non tumor cells contribute to efficacy and resistance of RASi. Taken together, this proposal integrates expertise in PDAC pathobiology, tumor immunology, and applies novel genetic tools to unveil new mechanisms that underlie the efficacy and durability of RAS inhibition.

Illinois Arts Council Agency

Illinois Arts Council Agency provides grants to support arts and cultural programming, artist fellowships, arts education, and community-based arts projects across IL.

Illinois Arts Council Agency

Supports Illinois arts organizations, artists, and arts education programs through operational support, project grants, and touring grants.

Illinois Council on the Arts

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

Illinois Council on the Arts

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

NIGMS - National Institute of General Medical Sciences

Project Summery/Abstract Amid a public health crisis driven by antibiotic-resistant pathogenic bacteria, bacteriophages (phages), which naturally infect and kill bacteria, represent a promising alternative as antimicrobials. However, a significant challenge is posed by diverse bacterial immune mechanisms that resist phage infections. Overcoming this obstacle requires phages equipped with robust anti-immune capabilities. In this context, ΦKZ-like jumbophages (genomes > 200kb) have an exceptional ability to counter various bacterial nucleolytic immune systems throughout infection, with numerous family members targeting key Gram-negative pathogens. The jumbophage ΦKZ is a broad host range killer of the multi-antibiotic-resistant pathogen Pseudomonas aeruginosa and serves as the leading model phage for this family. Immune evasion is largely achieved through the assembly of a bacterial membrane lipid derived compartment termed the “Early Phage Infection Vesicle” (EPIV), which I co-discovered during my postdoctoral work, and a phage-encoded proteinaceous compartment called the “phage nucleus,” which shields the replicating phage genome. The long term goal of this study is to understand three unexplored aspects of jumbophage biology related to the biogenesis and functioning of the EPIV. The EPIV houses early transcription, but the phage has to solve a fundamental challenge not previously solved in bacteria–mRNA export from a lipid-bound compartment and successful docking with ribosomes, which are unusually uncoupled from transcription in this case. I hypothesize that a novel mRNA export channel, analogous to the eukaryotic nuclear pore complex, is assembled by injected ΦKZ proteins to export mRNA to ribosomes. I will uncover this complex using cryo-ET, mass spectrometry and genetics. I will additionally examine the role of EPIV assembly in enabling ‘pseudolysogeny’ in jumbophage infections. This process of phage quiescence was observed in jumbophages long ago but lacks a mechanistic understanding. I hypothesize that the EPIV has the potential to be a stable pseudolysogenic entity inside an infected bacterium that I will test herein with my multidisciplinary approach. Finally, I will attempt to elucidate the mechanism of EPIV biogenesis – it remains entirely unknown how this massive membrane-bound organelle is rapidly assembled within bacteria and how its formation is conserved across diverse jumbophage infections. To answer these questions, I will combine genetic dissection and c-ET to reveal the key participants and early assembly events of this unique phage-driven prokaryotic organelle formation. Overall, my studies stand to uncover fundamentally fascinating bacterial-phage cell biology in addition to innovative and potentially transferable mechanisms to enhance phage success in combating pathogenic bacteria. This research will be conducted at UCSF, which hosts state-of-the-art facilities and a highly intellectual and collaborative research community. It will also provide me with the training in genetics and structural biology that I need to fulfill my postdoctoral training goals and pioneer an independent research program in bacterial-phage interactions.

NIGMS - National Institute of General Medical Sciences

PROJECT ABSTRACT: The mechanism and regulation of protein synthesis determines the diversity and capacity of the cellular proteome. At the center of this regulation is the ribosome - a megadalton RNA-protein complex composed of two-subunits – which integrates a wide variety of cellular signals. The ribosome’s exquisite sensitivity to regulatory cues is underscored by the fact that the majority of clinically used antibiotics exert their effect by either dysregulating or blocking specific aspects of the protein synthesis mechanism. Understanding the kinetic and structural basis of protein synthesis promises to elucidate core paradigms of gene expression control and to inform strategies for addressing the global threat posed by drug-resistant and emerging pathogens. Moreover, given that loss of translational control is a hallmark of cancer, a mechanistic understanding of ribosome function holds significant promise for developing novel small-molecule therapies, which are currently lacking in the treatment of human disease. Historically, investigations into structure-function relationships governing the protein synthesis mechanism have focused on bacterial systems approaches. Comparable studies in human systems have been hindered by the demand for large amounts of homogeneous protein synthesis machinery. As a result, the molecular distinctions between bacterial and mammalian protein synthesis - which underpin antibiotic specificity and potential therapeutic windows – remain obscure. Current evidence suggests that the elongation phase of protein synthesis, during which messenger RNA (mRNA) is decoded into protein, is the most time consuming, physiologically regulated and small-molecule sensitive. We and others hypothesize that elongation is particularly susceptible to regulation because it involves transient, repetitive interactions of the ribosome with auxiliary factors, coordinated through finely tuned conformational transitions that are acutely sensitive to perturbation. Small effects on many individual steps compound to exert large impacts on protein production. The proposed research seeks to rigorously and robustly define and quantify the elemental reactions underpinning the elongation phase of protein synthesis in bacteria and human. Our objectives are to: 1) elucidate the conserved mechanistic principles and divergent features of protein synthesis across evolution to define paradigms for selective control; 2] identify novel strategies for more effective antibiotic interventions for the treatment of infectious disease; and 3] evaluate the therapeutic potential of targeting dysregulated translation in cancer. To achieve these goals, we will deploy a suite of advanced biophysical methodologies - including single- molecule fluorescence imaging and state-of-the-art cryo-electron microscopy - to establish comprehensive and integrated kinetic and structural frameworks defining the elemental steps of elongation in bacteria and humans. The insights gained will advance our understanding of translation control, reveal atomic-resolution descriptions of drug actions on bacterial and human ribosomes, and inform new strategies for improving the efficacy of clinical treatments for both microbial and human disease.

NIAID - National Institute of Allergy and Infectious Diseases

ABSTRACT People living with Human Immunodeficiency virus (HIV) are up to 20 times more likely to develop active tuberculosis (TB) than people without HIV (PWoH). While anti-retroviral therapy (ART) has increased their health and lifespan, people with HIV (PWH) on ART are still at 4-5 fold greater risk for developing TB following infection with Mycobacterium tuberculosis (Mtb) compared to people without HIV (PWoH). However, why viral suppression and CD4 reconstitution following ART do not fully abrogate the risk of TB remains unclear. Residual inflammation present in PWH on ART has been linked to increased risk of co-infections and comorbidities. In addition, several lines of evidence show that PWH on ART have alterations in cellular metabolism, mainly within myeloid compartments, suggesting compromised abilities to mount effective immune responses to pathogens. A population of immunosuppressive cells termed myeloid-derived suppressor cells (MDSCs) has been implicated in dysfunctional immunity to HIV and Mtb infection. MDSCs were first described in cancer as negatively regulating tumor environments and suppressing NK and T cell functions. Higher frequencies of monocytic MDSCs (M- MDSC) were reported in PWH compared to PWoH, and M-MDSCs have been shown to expand after interruption of ART. Interestingly, M-MDSCs are also induced following Mtb infection but their role in anti-TB imunity in PWH on ART are not understood. We hypothesize that M-MDSCs suppress T cell functions and promote dysregulated immunometabolic responses to Mtb in PWH on ART. We propose to leverage bio-banked cryopreserved PBMC samples available through the Emory Center for AIDS research (CFAR) and our own archived samples, including from people with active and latent TB, with and without HIV. In Aim 1 we will employ multi-omic and immunologic approaches to derive an integrated MDSC biosignature associated with their suppressive functions and evaluate MDSC signature and frequencies in ART-naïve PWH, PWH on ART and PWoH. In Aim 2 we will test the hypothesis that expansion of M-MDSCs in PWH on ART contributes to ineffective immunity against Mtb-infection and promotes immunometabolic dysregulation. Our studies will bridge major knowledge gaps and provide a framework for targeting MDSCs to improve ART and advance HIV cure.